Peripheral blood lymphocyte subsets in children with nephrotic syndrome: a retrospective analysis.

BACKGROUND: Nephrotic syndrome (NS) in children is widely believed to be associated with severe changes in the immune system. Based on lymphocyte subset analysis, we examined the pathogenesis of immune deficiencies in children with NS with varying steroid sensitivity. METHODS: Our study utilized flow cytometry to retrospectively analyze the ratios of lymphocyte subsets in 204 children with nephrotic syndrome and 19 healthy children. RESULTS: Compared with healthy children, the ratio of CD4 + /CD8 + in onset and remission was decreased in SRNS group (p < 0.05), and CD19 + B lymphocytes were increased in onset (p < 0.05). Compared with onset, the proportion of CD19 + B lymphocytes decreased in SRNS, while the proportion of CD19 + B lymphocytes increased in SDNS, p < (0.01). The ratio of CD8 + T/CD19 + B in onset in SDNS group was significantly higher than that in SSNS and SRNS groups (p < 0.01) and healthy control group (p < 0.05). Compared with onset, the ratio of CD8 + T/CD19 + B in SDNS group decreased significantly (p < 0.01), while the ratio of CD8 + T/CD19 + B in SRNS group increased significantly (p < 0.01). The proportion of CD56 + CD16 + NK cells was significantly reduced in children with INS (p < 0.01). CONCLUSION: CD8 + T lymphocytes may be involved in the mechanism of lymphocyte subsets disorder during onset of SDNS, while CD19 + B lymphocytes may be involved in the mechanism of lymphocyte subsets disorder during relapse of SDNS. The CD8 + T/CD19 + B ratio may predict the degree of frequent recurrence. There is a certain degree of lymphoid subsets disorder in children with NS.

Diagnostic value of platelet-lymphocyte ratio and hemoglobin-platelet ratio in patients with rectal cancer.

BACKGROUND: This study aimed to investigate the diagnostic value of platelet-lymphocyte ratio (PLR) and hemoglobin-platelet ratio (HPR) combined or not with carcinoembryonic antigen (CEA) in rectal cancer. METHODS: We recruited 235 patients pathologically diagnosed with rectal cancer, 113 patients with benign rectal diseases, and 229 healthy control patients in this retrospective analysis. Then, the correlation between PLR, HPR, and clinicopathological findings was analyzed. Receiver operating characteristic (ROC) curve was used to assess the diagnostic value of PLR and HPR combined or not with CEA in rectal cancer patients. RESULTS: The levels of PLR, HPR, and CEA were higher in rectal cancer patients than those in the subjects with benign rectal diseases (P < .001) and the healthy controls (P < .001). Platelet-lymphocyte ratio and HPR were associated with lymph node metastasis and tumor stage, rather than serosa invasion, distant metastasis, or tumor size. PLR or HPR combined with CEA produced larger area under curve (AUC) (AUCPLR+CEA  = 0.75, 95% CI = 0.70-0.79, AUCHPR+CEA  = 0.76, 95% CI = 0.71-0.80) than PLR (P < .0001), HPR (P < .0001), or CEA (P = .024) alone. CONCLUSION: Our results suggest that PLR or HPR combined with CEA can increase diagnostic efficacy and may be a useful diagnostic marker for patients with rectal cancer.

Glycoprofiling of Early Gastric Cancer Using Lectin Microarray Technology.

BACKGROUND: Recently, studies have reported that protein glycosylation plays an important role in the occurrence and development of cancer. Gastric cancer is a common cancer with high morbidity and mortality owing to most gastric cancers are discovered only at an advanced stage. Here, we aim to discover novel specific serum glycanbased biomarkers for gastric cancer. METHODS: A lectin microarray with 50 kinds of tumor-associated lectin was used to detect the glycan profiles of serum samples between early gastric cancer and healthy controls. Then lectin blot was performed to validate the differences. RESULTS: The result of the lectin microarray showed that the signal intensities of 13 lectins showed significant differences between the healthy controls and early gastric cancer. Compared to the healthy, the normalized fluorescent intensities of the lectins PWA, LEL, and STL were significantly increased, and it implied that their specifically recognized GlcNAc showed an especially elevated expression in early gastric cancer. Moreover, the binding affinity of the lectins EEL, RCA-II, RCA-I, VAL, DSA, PHA-L, UEA, and CAL were higher in the early gastric cancer than in healthy controls. These glycan structures containing GalNAc, terminal Galß 1-4 GlcNAc, Tri/tetraantennary N-glycan, ß-1, 6GlcNAc branching structure, α-linked fucose residues, and Tn antigen were elevated in gastric cancer. While the two lectins CFL GNL reduced their binding ability. In addition, their specifically recognized N-acetyl-D-galactosamine structure and (α-1,3) mannose residues were decreased in early gastric cancer. Furthermore, lectin blot results of LEL, STL, PHA-L, RCA-I were consistent with the results of the lectin microarray. CONCLUSIONS: The findings of our study clarify the specific alterations for glycosylation during the pathogenesis of gastric cancer. The specific high expression of GlcNAc structure may act as a potential early diagnostic marker for gastric cancer.

Coffee consumption and prostate cancer risk: an updated meta-analysis.

PURPOSE: Many epidemiological studies have been conducted to explore the association between coffee consumption and prostate cancer. However, the results remain inconsistent. We performed a large meta-analysis of relevant studies to derive a more precise estimation of this relationship. METHODS: Systematic searches of PubMed and several other databases up to June 2013 were retrieved. All epidemiologic studies regarding coffee consumption and prostate cancer risk were included, and odds ratios (ORs) with 95 % confidence intervals (CIs) were calculated to estimate the strength of the association. RESULTS: Twelve case-control studies involving 7,909 prostate cancer cases and 9,461 controls and nine cohort studies involving 455,123 subjects were included in our analysis. Compared with the lowest category, the unstratified highest category of coffee consumption showed a significance reduction in prostate cancer risk of a fixed-effects model (OR 0.91, CI 0.86-0.97). A borderline significant influence was also found when the stratified highest category (US ≥ 4, Europe ≥ 5) of coffee consumption was compared with the reference category (OR 0.96, CI 0.92-1.00), but no relationships were observed for the other two categories. In another analysis conducted by coffee consumption and prostate cancer stage and Gleason grade, our results showed a significant inverse association in all categories of prostate cancer except Gleason <7 grade in a fixed-effects model; the results remained the same, except for advanced prostate cancer, in a random-effects model. CONCLUSIONS: Our meta-analysis suggests that high (e.g., highest ≥ 4 or 5 cups/day) coffee consumption may not only be associated with a reduced risk of overall prostate cancer, but also inversely associated with fatal and high-grade prostate cancer.

DNA repair gene XRCC3 polymorphisms and bladder cancer risk: a meta-analysis.

The X-ray repair cross-complementing group 3 (XRCC3) in homologous recombination repair (HRR) pathway plays a vital role in DNA double-strand break repair (DSBR). Variants in the XRCC3 gene might result in altered protein structure or function which may influence DSBR efficiency and lead to cancer. Numerous epidemiological studies have been conducted to evaluate the association between XRCC3 polymorphisms and bladder cancer risk. However, the results of these previous studies have been inconsistent. To derive a more precise estimation of the association, we performed a meta-analysis of all available studies relating XRCC3 polymorphisms and bladder cancer. All studies published up to April 2013 on the association between XRCC3 polymorphisms and bladder cancer risk were identified by searching electronic databases PubMed, EMBASE, and Chinese Biomedical Literature databases. The association between the XRCC3 polymorphisms and bladder cancer risk was assessed by odds ratios (ORs) together with their 95% confidence intervals (CIs). A total of 16 case-control studies met the inclusion criteria and were selected. With respect to C18067T polymorphism, significant increased bladder cancer risk was found when all eligible studies were pooled into the meta-analysis (TT vs. CC: OR = 1.174, 95%CI = 1.033-1.335, P = 0.014 and recessive model TT vs. TC + CC: OR = 1.147, 95%CI = 1.020-1.290, P = 0.022, respectively). The results were still significant after excluding the Hardy-Weinberg equilibrium violation studies (TT vs. CC: OR = 1.178, 95%CI = 1.036-1.339, P = 0.013 and recessive model TT vs. TC + CC: OR = 1.144, 95%CI = 1.017-1.287, P = 0.025, respectively). In subgroup analysis by ethnicity, significant elevated risk was found among Asians (dominant model TT + TC vs. CC: OR = 1.285, 95%CI = 1.012-1.631). In the subgroup analyses according to smoking status, no significant association was detected in all genetic comparison models. With respect to A17893G and A4541G polymorphisms, no significant association with bladder cancer risk was observed in the overall and subgroup analyses. This meta-analysis suggests that the XRCC3 C18067T polymorphism was associated with increased bladder cancer risk especially among Asians. However, the XRCC3 A17893G and A4541G polymorphisms may not play important roles in bladder carcinogenesis. Further studies with larger sample sizes are needed to validate our finds.

Lack of association between vitamin D receptor gene ApaI, BsmI, and TaqI polymorphisms and primary biliary cirrhosis risk: a meta-analysis.

Previous studies have reported the association between vitamin D receptor (VDR) polymorphisms and the risk of primary biliary cirrhosis (PBC), although these results remain controversial. The aim of this meta-analysis was to evaluate the association of three polymorphisms in VDR with PBC risk. The relevant studies were identified through an electronic database search carried out in September 2013. The crude odds ratio (OR) and 95% confidence interval (CI) were calculated to assess the association between VDR polymorphisms and PBC risk. Six eligible studies which met our selection criteria were included. Overall, the ApaI, BsmI, and TaqI polymorphisms in the VDR gene were not associated with PBC risk (ApaI A vs a OR = 1.132, 95% CI = 0.870-1.472, p = 0.355; BsmI B vs b OR = 1.148, 95% CI = 0.697-1.891, p = 0.589; TaqI t vs T OR = 1.1432, 95% CI = 0.709-1.841, p = 0.584). Furthermore, in subgroup analysis by ethnicity for the ApaI, BsmI, and TaqI polymorphisms, there were no significant results in either Caucasians or Asians under the allele contrast and recessive and dominant models. This meta-analysis indicated that VDR polymorphisms were not a risk factor for PBC. Larger and more carefully designed studies are needed to verify our results.

The association of interleukin-16 gene polymorphisms with IL-16 serum levels and risk of nasopharyngeal carcinoma in a Chinese population.

Interleukin (IL)-16 plays a fundamental role in inflammatory diseases, as well as in the development and progression of tumors. Genetic variation in DNA sequence of IL16 gene may lead to altered cytokine production and/or activity, and this variation may modulate an individual's susceptibility to nasopharyngeal carcinoma (NPC). To test this hypothesis, we investigated the association of IL16 gene polymorphisms and serum IL-16 levels with NPC risk in a Chinese population. We analyzed IL16 gene rs11556218 T/G, rs4778889 T/C, and rs4072111 C/T polymorphisms using PCR-RFLP and DNA sequencing, and serum IL-16 levels were measured by ELISA. The IL16 rs11556218 T/G polymorphism was significantly associated with the susceptibility to NPC patients. The TG genotype was associated with a significantly higher risk of NPC as compared with the TT genotype (OR = 2.05, 95% CI 1.04-4.01; p = 0.037). Patients carrying the G allele had a significantly higher risk for developing NPC compared with individuals carrying the T allele (OR = 1.79, 95% CI 1.07-3.01; p = 0.027). The serum IL-16 levels were increased in NPC patients compared with controls (p < 0.01); the genotypes carrying the IL16 rs11556218 G variant allele were associated with increased serum IL-16 levels compared with the homozygous wild-type genotype in NPC patients (all p values <0.01). Our data suggested that IL16 rs11556218 T/G polymorphism was associated with increased susceptibility to NPC through increasing the production of serum IL-16 levels.

LAPTM4B polymorphism increases susceptibility to multiple cancers in Chinese populations: a meta-analysis.

BACKGROUND: Lysosome-associated protein transmembrane-4 beta (LAPTM4B) is a novel cancer-related gene. While recent studies have reported that the LAPTM4B polymorphism increased the susceptibility of several cancers, the results remain inconclusive. Therefore, we performed a meta-analysis to systematically summarize the possible association. RESULTS: The meta-analysis was conducted based on 17 studies in Chinese populations, including 4160 cases and 4148 controls. The relevant studies were searched through electronic databases updated in November 2013. The strength of association between the LAPTM4B polymorphism and susceptibility to multiple cancers was assessed by odds ratio (OR) and 95% confidence interval (95% CI).The meta-analysis results suggested that the LAPTM4B polymorphism was significantly associated with overall susceptibility to multiple cancers in all genetic models (*2 vs. *1, OR = 1.53, 95% CI = 1.37-1.70; *2/2 vs. *1/1, OR = 2.18, 95% CI = 1.72-2.75; *2/1 vs.*1/1, OR = 1.62, 95% CI = 1.41-1.86; *2/1 + *2/2 vs. *1/1, OR = 1.70, 95% CI = 1.47-1.97; *2/2 vs. *2/1 + *1/1, OR = 1.76, 95% CI = 1.50-2.05). Further subgroup analysis revealed a significant association between the LAPTM4B polymorphism and cancer susceptibility in the subgroups stratified by control source, cancer type, histopathologic differentiation, and TNM stage. CONCLUSIONS: This meta-analysis indicated that the LAPTM4B *2 allele was associated with increasing risk of multiple cancers, tumor initiation and development.

Lack of association between cathepsin D C224T polymorphism and Alzheimer's disease risk: an update meta-analysis.

BACKGROUND: Cathepsin D C224T polymorphism has been reported to associate with AD susceptibility. But the results were inconsistent. This study aimed to assess the relationship between C224T polymorphism and AD risk. METHODS: The relevant studies were identified by searching PubMed, Embase, Web of Science, Google Scholar and Wan fang electronic databases updated on July 2013. The relationship between Cathepsin D C224T polymorphism and AD risk was evaluated by ORs and 95% CIs. RESULTS: A total of 25 case-control studies including 5,602 cases and 11,049 controls were included in the meta-analysis. There was no association between C224T polymorphism and AD risk with all the studies were pooled in the meta-analysis (CT vs. CC: OR = 1.125, 95% CI = 0.974-1.299, P = 0.109; CT + TT vs. CC: OR = 1.136, 95% CI = 0.978-1.320, P = 0.094). Furthermore, when stratified by ethnicity, age of onset and APOEϵ4 status, significant association did not found in all subgroups. CONCLUSION: The present meta-analysis suggested that the Cathepsin D C224T polymorphism was not associated with AD susceptibility.

Determination of reference intervals for serum complement C3 and C4 levels in Chinese Han ethnic males.

BACKGROUND: Clinical laboratory reference intervals (RIs) for serum complement C3 and C4 levels have been established in many countries but there is a lack of published data regarding normal RIs in Chinese population. We attempted to establish RIs for serum complement C3 and C4 levels in Chinese Han ethnic males. METHODS: A total of 1,234 healthy male subjects, aged 20 - 69 years, were collected from the Fangchenggang Area Male Health and Examination Survey (FAMHES). Serum complement C3 and C4 levels were measured by immunoturbidimetry. The two-sided 95-percentile RIs were calculated using parametric statistical methods. RESULTS: Serum C3 values showed normal distribution and C4 were log-normal distributed. The two-sided 95% RIs (mean +/- 2 SD) for serum C3 and C4 were 0.656 - 1.52 g/L and 0.181 - 0.561 g/L, respectively. Body Mass Index (BMI) had a significant positive association with C3 (r = 0.342) and C4 (r = 0.258), and age had a significant positive association with C4 (r = 0.117). No significant difference was found either between smoking groups or drinking groups. A significant increase with BMI was found both for C3 (p < 0.001) and C4 (p < 0.001). BMI-specific RIs were also calculated. CONCLUSIONS: The RIs for serum C3 and C4 show a slight deviation compared to previously reported reference levels. BMI-specific reference values should be implemented in clinical laboratories.

Establishing reference values for blood urea nitrogen and serum creatinine in Chinese Han ethnic adult men.

BACKGROUND: The aim was to calculate the two-sided 95th percentile reference values for blood urea nitrogen (BUN) and serum creatinine (SCr) in Chinese Han ethnic adult men. METHODS: Serum samples were collected from Chinese Han ethnic adult men aged 20 - 69 years. After screening based on the inclusion and exclusion criteria, a total of 1575 individuals were enrolled in our study. BUN and SCr values were measured on an automatic analyzer (Dade Behring, USA). The data was analyzed and calculated using nonparametric statistical methods. RESULTS: BUN and SCr values were not normally distributed. The reference values were in the range 3.3 - 7.5 mmol/L for BUN and 64 - 113 micromol/L for SCr. BUN levels were significantly lower in the smoking group than the non-smoking group (Z = -4.52, p < 10(-5)). An increase with age was observed in BUN levels (r(s) = 0.172, p < 0(-5)) and lower SCr levels were weakly associated with the older subjects (r(s) = -0.071, p = 0.005). Moreover, it was found that higher Body Mass Index (BMI) tended toward higher levels of SCr (r(s) = 0.118, p < 10(-5)). CONCLUSIONS: The reference values established for BUN and SCr exhibit a slight deviation compared to those developed in previous studies. We propose reference values of BUN for smokers and non-smokers be constructed, and age- and BMI-specific reference values be applied in clinical laboratories.

Effect of polyethylene microplastics on antibiotic resistance genes: A comparison based on different soil types and plant types.

Microplastics (MPs) and antibiotic resistance genes (ARGs) are two types of contaminants that are widely present in the soil environment. MPs can act as carriers of microbes, facilitating the colonization and spread of ARGs and thus posing potential hazards to ecosystem safety and human health. In the present study, we explored the microbial networks and ARG distribution characteristics in different soil types (heavy metal (HM)-contaminated soil and agricultural soil planted with different plants: Bidens pilosa L., Ipomoea aquatica F., and Brassica chinensis L.) after the application of MPs and evaluated environmental factors, potential microbial hosts, and ARGs. The microbial communities in the three rhizosphere soils were closely related to each other, and the modularity of the microbial networks was greater than 0.4. Moreover, the core taxa in the microbial networks, including Actinobacteriota, Proteobacteria, and Myxococcota, were important for resisting environmental stress. The ARG resistance mechanisms were dominated by antibiotic efflux in all three rhizosphere soils. Based on the annotation results, the MP treatments induced changes in the relative abundance of microbes carrying ARGs, and the G1-5 treatment significantly increased the abundance of MuxB in Verrucomicrobia, Elusimicrobia, Actinobacteria, Planctomycetes, and Acidobacteria. Path analysis showed that changes in MP particle size and dosage may indirectly affect soil enzyme activities by changing pH, which affects microbes and ARGs. We suggest that MPs may provide surfaces for ARG accumulation, leading to ARG enrichment in plants. In conclusion, our results demonstrate that MPs, as potentially persistent pollutants, can affect different types of soil environments and that the presence of ARGs may cause substantial environmental risks.

Reference intervals for serum lipids in coastal males from Fangchenggang.

BACKGROUND: We aimed to establish the reference intervals for serum lipids in coastal residents of the Chinese male population. METHODS: A total of 1436 subjects, aged between 19 and 86 years, were selected from the Fangchenggang Area for Male Health and Examination Survey (FAMHES). Reference intervals of serum lipids were measured by enzymatic endpoint colorimetry and information was obtained using a standard questionnaire. RESULTS: The total nonparametric reference intervals for TC < 5.95 mmol/L (229.73 mg/dL), TG < 1.80 mmol/L (158.82 mg/dL), HDL-C > 1.90 mmol/L (73.08 mg/dL), and LDL-C < 3.37 mmol/L (130 mg/dL). High serum lipid levels were correlated with older age, higher body mass index (BMI), and more smoking, but not with alcohol consumption. CONCLUSIONS: The established reference intervals of serum lipids for coastal Chinese male residents would be helpful for assessing risk of cardiovascular disease. We recommend establishing population-based reference intervals for serum lipids in clinical laboratories.

Characteristics and clustering analysis of peripheral blood lymphocyte subsets in children with systemic lupus erythematosus complicated with clinical infection.

OBJECTIVES: Clinical infection is a common complication in children with systemic lupus erythematosus (SLE). However, few studies have investigated immune alterations in children with SLE complicated with clinical infection. We assessed lymphocyte subsets in children with SLE to explore the possibility of clinical infection. METHODS: We retrospectively analyzed the proportion of peripheral lymphocyte subsets in 140 children with SLE. Children with SLE were classified into different clusters according to the proportion of peripheral blood lymphocyte subsets: (CD3 + /CD4 + T cell, CD3 + /CD8 + T cell, CD3 + /CD4 + /CD8 + T cell, CD3 + /CD4-/CD8- T cell, CD19 + B cell, and CD3-/CD16 + /CD56 + NK cell). Differences in the proportion of lymphoid subsets, infection rates, and systemic lupus erythematosus disease activity index (SLEDAI) scores were compared between clusters. In addition, we grouped the subjects according to the presence or absence of infection. Proportions of lymphoid subsets, demographic variables, clinical presentation, and other laboratory variables were compared between the infected and uninfected groups. Finally, the diagnostic ability of lymphocyte subset ratios to distinguish secondary infection in children with SLE was predicted using an ROC curve. RESULTS: Cluster C2 had a higher proportion of B cells than Cluster C1, while Cluster C1 had a lower proportion of NK cells, CD3 + T cells, CD3 + /CD4 + T cells, CD3 + /CD8 + T cells, and CD3 + /CD4-/CD8- T cells. Infection rates and SLEDAI scores were higher in Cluster C2 than in Cluster C1. The infected children had a higher proportion of B cells and a lower proportion of CD3 + T cells, CD3 + /CD4 + T cells, CD3 + /CD8 + T cells, and CD3 + /CD4-/CD8- T cells. There were no significant differences in lymphoid subsets between children in Cluster C2 and the infected groups. The area under the ROC curve of B lymphocytes in predicting SLE children with infection was 0.842. The area under the ROC curve was 0.855 when a combination of B cells, NK cells, CD4 + T cells, and CD8 + T cells was used to predict the outcome of coinfection. CONCLUSIONS: A high percentage of B cells and a low percentage of CD3 + T cells, CD3 + /CD4 + T cells, CD3 + /CD8 + T cells, CD3 + /CD4 + /CD8 + T cells, and CD3 + /CD4-/CD8- T cells may be associated with infection in children with SLE. B cells was used to predict the outcome of coinfection in children with SLE. Key Points • A high percentage of B cells and a low percentage of CD3 + T cells, CD3 + /CD4 + T cells, CD3 + /CD8 + T cells, CD3 + /CD4 + /CD8 + T cells, and CD3 + /CD4-/CD8- T cells may be associated with infection in children with SLE • B cells was used to predict the outcome of coinfection in children with SLE.

Potential impact of polyethylene microplastics on the growth of water spinach (Ipomoea aquatica F.): Endophyte and rhizosphere effects.

Microplastic contamination has received much attention, especially in agroecosystems. However, since edible crops with different genetic backgrounds may present different responses to microplastics, more research should be conducted and focused on more edible crops. In the current study, pot experiments were conducted to investigate the potential impact of polyethylene microplastic (PE) (particle sizes: 0.5 µm and 1.0 µm, addition levels: 0 (control), 0.5% and 1.0% (w/w)) addition on the physiological and biochemical variations of I. aquatica F.. The results indicated that PE addition caused an increase in the soil pH and NH4+-N and soil organic matter contents, which increased by 10.1%, 29.9% and 50.1% when PE addition at A10P0.5 level (10 g (PE) kg-1 soil, particle size: 0.5 µm). While, PE exposure resulted in a decrease in soil available phosphorus and total phosphorus contents, which decreased by 53.9% and 10.5% when PE addition at A10P0.5 level. In addition, PE addition altered the soil enzyme activities. Two-way ANOVA indicated that particle size had a greater impact on the variations in soil properties and enzyme activities than the addition level. PE addition had a strong impact on the rhizosphere microbial and root endophyte community diversity and structure of I. aquatica F.. Two-way ANOVA results indicated that the particle size and addition level significantly altered the α-diversity indices of both rhizosphere microbial and root endophyte (P < 0.05, P < 0.01 or P < 0.001). Moreover, PE was adsorbed by I. aquatica F., which was clearly observed in the transverse roots and significantly increased the H2O2, ·O2-, malondialdehyde and ascorbic acid contents in both the roots and aerial parts of I. aquatica F., leading to a decrease in I. aquatica F. biomass. Overall, the current study enriches the understanding of the effect of microplastics on edible crops.

Testis-specific protein Y-encoded 1 regulates androgen receptor expression through the MAPK/ERK pathway in male hepatocellular carcinoma.

OBJECTIVES: To analyze the mechanism of testis-specific protein Y-encoded 1 (TSPY1) in male hepatocellular carcinoma (HCC). METHODS: This experimental study was carried out at Guangxi Medical University's First Affiliated Hospital, Guangxi, China, between January 2016 and December 2019. The expression of TSPY1, androgen receptor (AR), messenger ribonucleic acids (mRNAs), and proteins were detected by qRT-PCR and Western blotting. The co-localization and interaction of TSPY1 and AR were observed by immunofluorescence assay and co-immunoprecipitation. Hepatocellular carcinoma cells overexpressing and silencing TSPY1 were constructed, and the expression and phosphorylation levels of TSPY1, AR, and mitogen-activated protein kinases/extracellular signal-regulated kinases (MAPK/ERK) signaling pathway-related key molecules ERK1/2, p38, and JNK were also detected. RESULTS: The expression levels of TSPY1, AR mRNAs, and proteins were highly positively correlated in HCC cells in different metastatic potentials with a high correlation coefficient of R=0.929 and R=0.884. Testis-specific protein Y-encoded 1 and AR were then co-localized in the nucleus of HCC cells, and TSPY1 and AR can interact with each other. In addition, the expression of AR and phosphorylation of ERK1/2 were enhanced in TSPY1 overexpressed Huh7 cells. They were reduced in HCCLM3 cells with TSPY1 knockdown expression. In addition, in response to blocking MAPK/ERK signaling activity, AR was reduced in expression. CONCLUSION: These findings suggested that there was a positive correlation between TSPY1 expression and AR in male HCC cells, and high TSPY1 expression stimulates AR expression, MAPK/ERK signaling pathway may be involved in its mechanism.

Diagnostic value of long noncoding RNA LINC01485 in patients with colorectal cancer.

BACKGROUND: Long noncoding RNAs (lncRNAs) were considered as transcription noise without biological functions. However, accumulated evidence shows that lncRNAs are expressed heterogeneously in tumor tissues. This study aims to identify the specific expression of lncRNAs in colorectal cancer patients and to perform verification analysis. METHODS: The differentially expressed lncRNAs and mRNAs in colorectal cancer and normal tissues were screened by bioinformatics methods. Subsequently, the qRT-PCR method was used to verify the expression of differential lncRNAs in tumor tissues and blood samples. Concurrently ROC curves were used to analyze the diagnostic efficacy of lncRNAs. Moreover, the correlation between lncRNAs and clinicopathological features was also analyzed. Finally, functional annotation analysis was performed for lncRNAs. RESULTS: Eleven lncRNAs differentially expressed in colorectal cancer tissues and normal tissues were screened. In the validation tissue sample set, FOXD3-AS1 was down-regulated in colorectal cancer tissues (P < 0.001), while LINC01485 was up-regulated in colorectal cancer tissues compared with the adjacent tissues (P < 0.05). In a further verification of the whole blood sample set, LINC01485 showed high sensitivity and specificity (sensitivity = 98.33%, specificity = 84.00%) in differentiating colorectal cancer patients from healthy controls (P < 0.001). Simultaneously, there was no difference in the expression of LINC01485 in other gastrointestinal tumors (hepatocellular carcinoma, esophageal cancer, gastric cancer, and pancreatic cancer) and healthy controls. LINC01485 is significantly related to the clinical staging, lymph node metastasis, and distant metastasis of colorectal cancer. CONCLUSIONS: The expression, diagnostic efficiency, and functional analysis of the lncRNA file of colorectal cancer reveals the important role of LINC01485 in colorectal cancer and provides an important clinical reference value for the early diagnosis and targeted therapy of colorectal cancer.

Long Intergenic Non-Coding 00162 as Diagnostic Biomarker for Early-Stage Pancreatic Cancer.

OBJECTIVE: Pancreatic cancer (PC) is the fourth leading cause of cancer death due to insufficient diagnostic methods in early stage of PC. Growing evidence has shown that long intergenic non-coding RNAs (LINCRNAs) is a biomarker of the early-stage of PC. However, the expression level and diagnostic value of LINC00162 remains unclear. METHODS: LINC00162 expression was detected in peripheral blood samples from 155 subjects (52 healthy controls, 52 benign pancreatic disease (BPD) persons and 51 PC patients) by quantitative reverse transcription real-time polymerase chain reaction. Receiver operating characteristic (ROC) analysis was used to evaluate the diagnostic value of LINC00162, carcinoembryonic antigen (CEA) and cancer antigen 199 (CA199). RESULTS: Our data indicated that the LINC00162 expression was upregulated in PC patients compared with healthy controls and BPD (all P<0.001). Furthermore, PC patients with advanced pathological grades, positive lymph node metastasis and positive distant metastasis showed higher LINC00162 levels (all P<0.001). In addition, the area under the ROC curve (AUC) found that the LINC00162 had higher diagnostic ability than CEA and CA199 in distinguishing the early-stage PC patients (AUC: LINC00162 versus(vs) CEA vs CA199=0.932 vs 0.669 vs 0.725). CONCLUSION: In summary, the LINC00162 may be a noninvasive and efficient marker for identifying patients with the early-stage PC. Further validation studies with a large number of patients and long-term follow-up patients are needed to confirm the potential diagnostic value and clinical utility of LINC00162 in patients with PC.

Long non-coding RNA LINC01793 as a potential diagnostic biomarker of hepatitis B virus-related hepatocellular carcinoma.

BACKGROUND: There is growing evidence that long non-coding RNAs (lncRNAs) play important roles in the progression of hepatocellular carcinoma (HCC) and may serve as diagnostic markers. This study investigates the diagnostic efficiency of the long intergenic non-protein-coding RNA 1793 (LINC01793) in hepatitis B virus (HBV)-related HCC. METHODS: Bioinformatics methods were used to screen the aberrantly expressed lncRNAs in HCC tissues based on The Cancer Genome Atlas (TCGA). Quantitative reverse transcription polymerase chain reaction was performed to assess the expression of the candidate lncRNAs in tissues, cells and whole blood samples of patients with HBV-related HCC, liver cirrhosis (LC), chronic hepatitis (CHB), and healthy controls. Then, the correlations between LINC01793 and clinical characteristics were analyzed. Finally, the diagnostic value of LINC01793 was explored based on the receiver operating characteristic curve. RESULTS: LINC01793 was remarkably upregulated in the HCC tissues and cells. It was highly expressed in the whole blood of the HBV-related HCC patients, unlike in that of the healthy controls and of the CHB and LC patients. Subsequent analysis revealed that high LINC01793 was related to the Barcelona Clinic Liver Cancer (P = 0.007), tumor invasion (P = 0.042), the number of tumors (P = 0.031) and serum level of alanine aminotransferase(p = 0.022). The areas under the curve of LINC01793, for distinguishing HCC from healthy controls, CHB and LC patients, were 0.824, 0.767 and 0.756, respectively. In addition, the combination of LINC01793 with alpha fetoprotein (AFP) had a stronger diagnostic value than LINC01793 or AFP alone in AFP-negative HCC patients. CONCLUSION: High expression of LINC01793 is correlated with adverse clinical characteristics and can serve as a non-invasive biomarker of HCC.

Genetic polymorphisms in complement receptor 1 gene and its association with HBV-related liver disease: A case-control study.

BACKGROUND: Several investigators have reported that complement receptor 1 (CR1) likely play a role in the pathogenesis of tumors, autoimmune and inflammatory diseases. However, the association of genetic polymorphisms of CR1 with risk of hepatitis B virus (HBV)-related liver disease remains unexplored. METHODS: In a case-control study of 399 HBV-related liver disease patients and 227 healthy controls, we genotyped two SNPs in CR1 (rs3811381 and rs2274567) and assessed their associations with risk of HBV-related liver disease. RESULTS: No significant differences were observed in the frequency distribution of genotypes or alleles between CR1 rs3811381 and rs2274567 polymorphisms in patients and controls. However, stratification analysis indicated that these two CR1 polymorphisms may contribute to the risk of HBV- hepatocellular carcinoma (HCC) and chronic hepatitis B (CHB) in subgroups of males, alcohol drinkers and nonsmokers. Further, our results showed that the rs3811381 polymorphism may contribute to HBV-HCC risk in subgroups of older and younger subjects, while the G allele, AG and the combined AG + GG genotypes of rs2274567 may be risk factors for HBV-HCC in younger subjects. In addition, our results indicated that subjects who carried the rs3811381 G allele and the rs2274567 AG genotype were at decreased risk of HBV- liver cirrhosis (LC) in subgroups of females. CONCLUSIONS: Our results support the hypothesis that the CR1 gene rs3811381 and rs2274567 polymorphisms may contribute to HBV-HCC and HBV-CHB risk, particularly in subgroups of males, alcohol drinkers, nonsmokers, while these two CR1 polymorphisms were found to associate with decreased risk of HBV-LC, particularly in females. Further validation of these results is warranted.