Glyoxal damages human aortic endothelial cells by perturbing the glutathione, mitochondrial membrane potential, and mitogen-activated protein kinase pathways.

BACKGROUND: Exposure to glyoxal, the smallest dialdehyde, is associated with several diseases; humans are routinely exposed to glyoxal because of its ubiquitous presence in foods and the environment. The aim of this study was to examine the damage caused by glyoxal in human aortic endothelial cells. METHODS: Cell survival assays and quantitative fluorescence assays were performed to measure DNA damage; oxidative stress was detected by colorimetric assays and quantitative fluorescence, and the mitogen-activated protein kinase pathways were assessed using western blotting. RESULTS: Exposure to glyoxal was found to be linked to abnormal glutathione activity, the collapse of mitochondrial membrane potential, and the activation of mitogen-activated protein kinase pathways. However, DNA damage and thioredoxin oxidation were not induced by dialdehydes. CONCLUSIONS: Intracellular glutathione, members of the mitogen-activated protein kinase pathways, and the mitochondrial membrane potential are all critical targets of glyoxal. These findings provide novel insights into the molecular mechanisms perturbed by glyoxal, and may facilitate the development of new therapeutics and diagnostic markers for cardiovascular diseases.

Predictive value of vascular endothelial growth factor polymorphisms on the risk of renal cell carcinomas: a case-control study.

We conducted this case-control study to assess the role of vascular endothelial growth factor (VEGF) -2578C/A, +460T/C, +1612G/A, +936C/T, and -634G/C polymorphisms in the development of renal cell carcinoma (RCC), and analyzed the association of gene polymorphisms with demographic and clinical characteristics of RCC. This study included 412 consecutive primary RCC patients and 824 controls. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed to detect VEGF -2578C/A, +460T/C, +1612G/A, +936C/T, and -634G/C polymorphisms. Compared with the control subjects, the RCC cancer cases were more likely to have a habit of cigarette smoking, and suffered from hypertension and diabetes. Conditional logistic regression analysis showed that individuals carrying the AA genotype of -2578C/A were more likely to greatly increase risk of RCC, and the CC genotype of +460T/C revealed a significant association with increased risk of RCC. The CA + AA genotype of -2578C/A had a significantly increased risk of RCC in ever cigarette smokers, and individuals who suffered from hypertension and diabetes. TC + CC genotype of +460T/C was significantly associated with the elevated risk of RCC in those suffered from hypertension and diabetes. Our study suggests that -2578C/A and +460T/C polymorphisms of VEGF modulate the risk of developing RCC in Chinese population.

High serum miR-183 level is associated with poor responsiveness of renal cancer to natural killer cells.

Renal cell carcinoma (RCC) is among the most common subtype of kidney cancers, and the current therapeutic strategies are not efficient. Natural killer (NK) cells are biological agents that can induce apoptosis in a wide range of cancer cells. However, most of RCC patients exhibit resistance against the action of NK cells due to unknown mechanisms. This study is aimed to identify a biomarker that can predict the response of RCC cells to NK cell treatment. We collected 82 RCC patients and 19 healthy volunteers to detect the expression of miR-183 in blood by qPCR assays. The results revealed that serum miR-183 is significantly higher in RCC patients than in healthy controls, and its level is positively associated with the grading of RCC. Furthermore, (51)Cr release assays indicated that the primary RCC cells with low serum miR-183 expression are more sensitive to the cytotoxicity of NK cells. Collectively, we demonstrated that serum miR-183 can be used to predict the response of RCC cells to the cytotoxicity induced by NK cells.

An infectious molecular clone in early infection with HIV-1 subtype CRF01_AE strains: construction and biological properties.

Our aim was to construct infectious molecular clones of the CRF01_AE subtype in the primary infection phase of an acute HIV-1 infections in people screened from MSM populations, as well as continue preliminary research on this virus and its biological properties pertaining to deriving viruses. Walking sequencing was performed on a half-molecular clone with target fragment inserted. Western Blot was used to detect protein expression in HIV-1 infected 293T cells. Sequence analysis of HIV-1 genomic clones showed full-length HIV-1 genomic clones without frame shift mutation or termination codon. HIV-1 p24 antigens generated from 08-IMC were slightly greater than those from infectious molecular clones pNL4-3 3 and 93JP-NH1, but without statistical difference (all P > 0.05). The relative light units of 08-ISO was higher than those of 08-IMC, but no significant difference was observed (all P > 0.05). 08-IMC-driven virus was linked to lower replication kinetics. The replication levels of pNL4-3 and 08-ISO were significantly higher than the 08-IMC replication level but close to NH1 replication level (all P < 0.05). 08-IMC could infect the cells expressing CCR5 and be replicated in the CCR5-expressing cells with a positive percentage of 24.3 %, 08-ISO may use CCR5-using macrophage-tropic isolates as coreceptor, while pNL4-3 viruses with T cell tropisms utilize the CXCR4 co-receptor. Our study showed that the infectious molecular clones of viruses in the primary infection phase have a close relationship with the major prevalent CRF01_AE strains and have high homology with the viral RNA in plasma.

HIF-1α knockdown suppresses breast cancer metastasis via epithelial mesenchymal transition Abrogation.

Lung metastasis, a leading cause of breast cancer mortality, lacks effective therapeutic options. Hypoxia-inducible factor 1-alpha (HIF-1α) plays important roles in breast cancer progression, but its direct impact on lung metastasis remains unclear. Herein, in this study, we investigated the role of HIF-1α in breast cancer lung metastasis and the potential of targeting it for therapeutic benefit. HIF-1α expression was knocked down in the 4T1 mouse mammary carcinoma cell line using a lentiviral vector. HIF-1α knockdown significantly reduced the migratory ability of 4T1 cells in vitro and lung metastasis in a mouse model. Mechanistically, HIF-1α knockdown decreased the expression of matrix metalloproteinases (MMP-2 and MMP-9) that degrade the extracellular matrix and suppressed the epithelial-to-mesenchymal transition (EMT) by increasing E-cadherin and decreasing vimentin expression. The findings of this study demonstrate that HIF-1α knockdown effectively inhibits lung metastasis of 4T1 cells both in vitro and in vivo by suppressing EMT. These results underscore a promising new approach for managing breast cancer metastasis.

[Urinary neutrophil gelatinase-associated lipocalin (uNGAL) and early diagnosis of paraquat poisoning patients with acute kidney injury].

OBJECTIVE: To explore the use of the urinary neutrophil gelatinase associated lipocalin (uNGAL) in the early diagnosis of paraquat poisoning patients with acute kidney injury (AKI). METHODS: Eighty five patients were from the emergency department in our hospital. Five ml blood and urine were collected from each patient at 15 min, 2, 4, 6, 8, 10, 12, 18, 24, 36, 48 and 72 h, 5 and 7d after admission. The uNGAL levels of urine were detected with ELISA test and the SCr levels were measured with creatine oxidase assay. RESULTS: Sixty two cases of paraquat intoxication suffered from AKI, the incidence was 72.94% (62/85). The SCr levels of 62 cases with AKI at 18, 24, 36, 48, 72 h and 5, 7 d after admission increased significantly, as compared with the baseline value and control group (P < 0.01). At 24, 36, 48, 72 h and 5, 7 d after admission, there was significant difference of the SCr levels between AKI group and non-AKI group (P < 0.01). At 2 h after admission, the uNGAL level of urine in paraquat intoxication AKI group was (96.21 +/- 45.32) microg/L which was significantly higher than the baseline value. At 10, 12, 18, 24, 36, 48, 72 h and 5, 7 d after admission, the uNGAL levels of urine in AKI group and non-AKI group obviously enhanced, as compared with the baseline value and control group (P < 0.01 or P < 0.05). At all time points, there was significant difference of the uNGAL level between AKI group and non-AKI group (P < 0.01). CONCLUSION: The uNGAL level of urine in paraquat intoxication patients at 2 h after admission significantly enhanced, which is earlier than enhanced SCr. So the uNGAL level of urine may serve as early diagnostic biomarker for AKI induced by paraquat intoxication.

[Clinical study of dynamic change of inflammatory factors in serum of acute paraquat rats].

OBJECTIVE: To investigate the change of inflammatory factor in lung tissue of acute paraquat (PQ) poisoned rats. METHODS: hundred SD rats were randomly divided into two groups: the normal control group (NC group, n = 10) and the PQ group (n = 80). The 1 ml saline was administered once in normal control group. The PQ group was administered with 25 mg/kg 1% PQ by intraperitoneal injection to establish the model of PQ induced renal injury. At six hours, at the first, the third and the seventh day the PQ group were sacrificed, while at the first day the normal control group was sacrificed. The level of normal tumor necrosis factor-α (TNF-α), interleukin-2 (IL-2), IL-6 in serum of rats were detected. Meanwhile, pathological changes of the renal were examined under optical microscope. RESULTS: Histopathological findings of an earlier, a large number of patients edema clearly inflammatory cell infiltration. Compared with the control group, PQ exposure of serum TNF-α, IL-2, IL-6, the level at each time point were elevated. PQ treated group 6 h and 1, 3, 7 d when the IL-2 levels were (2.16 ± 0.65), (2.95 ± 1.02), (3.05 ± 1.12), (2.21 ± 0.62) µg/L, IL-6 were (62.5 ± 8.6), (85.6 ± 13.5), (90.3 ± 15.6), (65.3 ± 9.1) ng/ml, TNF-α were (1.95 ± 0.53), (2.86 ± 0.92), (3.15 ± 1.02), (2.06 ± 0.71) µg/L, compared with the control group, are significantly higher, the differences were statistically significant (P < 0.01). CONCLUSION: acute PQ poisoning serum TNF-α, IL-2, IL-6 levels were significantly increased both early and late inflammatory factors involved in PQ poisoning the pathogenesis of renal injury.

Cancer-associated fibroblasts secreted miR-103a-3p suppresses apoptosis and promotes cisplatin resistance in non-small cell lung cancer.

BACKGROUND: The cisplatin resistance of non-small cell lung cancer (NSCLC) patients results in low response rate and overall survival rate. Exosomes contribute to pathological processes of multiple cancers. OBJECTIVE: In this study, we explored the function and mechanisms of exosomal miR-103a-3p derived from cancer-associated fibroblast (CAF) in cisplatin resistance in NSCLC. RESULTS: MiR-103a-3p was highly expressed in CAFs and CAF exosomes, and exosomal miR-103a-3p derived from CAFs in NSCLC. CAFs exosomes co-cultured with NSCLC cells promoted miR-103a-3p expression both in NSCLC cells and its exosomes. Functional experiments showed that exo-miR-103a-3p derived from CAFs promoted cisplatin resistance and inhibited apoptosis in NSCLC cells. Pumilio2 (Pum2) bound with miR-103a-3p in cytoplasm and nucleus, and facilitated packaging into CAF-derived exosomes in NSCLC cells. Further analysis showed Bak1 was a direct target of miR-103a-3p, and miR-103a-3p accelerated cisplatin resistance in NSCLC cells via Bak1 downregulation. In vivo tumorigenesis assay showed CAF-derived exosomal miR-103a-3p enhanced cisplatin resistance and inhibited cell apoptosis in NSCLC. CONCLUSION: Our study revealed that CAFs-derived exosomal miR-103a-3p promoted cisplatin resistance by suppressing apoptosis via targeting Bak1, which provided a potential therapeutic target for cisplatin resistance in NSCLC.

MicroRNA-132-3p suppresses type I IFN response through targeting IRF1 to facilitate H1N1 influenza A virus infection.

Increasing evidence has indicated that microRNAs (miRNAs) have essential roles in innate immune responses to various viral infections; however, the role of miRNAs in H1N1 influenza A virus (IAV) infection is still unclear. The present study aimed to elucidate the role and mechanism of miRNAs in IAV replication in vitro. Using a microarray assay, we analyzed the expression profiles of miRNAs in peripheral blood from IAV patients. It was found that miR-132-3p was significantly up-regulated in peripheral blood samples from IAV patients. It was also observed that IAV infection up-regulated the expression of miR-132-3p in a dose- and time-dependent manner. Subsequently, we investigated miR-132-3p function and found that up-regulation of miR-132-3p promoted IAV replication, whereas knockdown of miR-132-3p repressed replication. Meanwhile, overexpression of miR-132-3p could inhibit IAV triggered INF-α and INF-ß production and IFN-stimulated gene (ISG) expression, including myxovirus protein A (MxA), 2',5'-oligoadenylate synthetases (OAS), and double-stranded RNA-dependent protein kinase (PKR), while inhibition of miR-132-3p enhanced IAV triggered these effects. Of note, interferon regulatory factor 1 (IRF1), a well-known regulator of the type I IFN response, was identified as a direct target of miR-132-3p during HIN1 IAV infection. Furthermore, knockdown of IRF1 by si-IRF1 reversed the promoting effects of miR-132-3p inhibition on type I IFN response. Taken together, up-regulation of miR-132-3p promotes IAV replication by suppressing type I IFN response through its target gene IRF1, suggesting that miR-132-3p could represent a novel potential therapeutic target of IAV treatment.

MicroRNA­199a­5p functions as a tumor suppressor in oral squamous cell carcinoma via targeting the IKKß/NF­κB signaling pathway.

MicroRNAs (miRNAs) have been shown to have a significant role in the progression of several types of cancer, including oral squamous cell carcinoma (OSCC). However, the biological function and regulatory mechanisms of miRNAs in OSCC remain to be fully elucidated. The aim of the present study was to investigate the role of miRNAs in OSCC and the relevant mechanism. Using a microarray, it was found that miRNA (miR)­199a­5p was one of the most downregulated miRNAs in OSCC tissues. A low expression of miR­199a­5p was closely associated with tumor differentiation, lymph node metastasis, tumor­node­metastasis stage, and overall survival rate. Functionally, the overexpression of miR­199a­5p suppressed cell proliferation, induced G0/G1 cell cycle arrest, and promoted the apoptosis of Tca8113 and SCC­4 cells. Subsequently, inhibitor of nuclear factor­κB (NF­κB) kinase ß (IKKß), an important regulator of NF­κB activation, was identified as a direct target of miR­199­5p. An inverse correlation was found between miR­199a­5p and IKKß in tumor tissues. Further investigations revealed that the overexpression of IKKß efficiently abrogated the influences caused by the overexpression of miR­199a­5p. It was also found that the miR­199a­5p­mediated anticancer effects were dependent on the inhibition of NF­κB activation. These findings indicate that miR­199a­5p functions as a tumor suppressor through regulation of the NF­κB pathway by targeting IKKß in OSCC.

MicroRNA­199a­5p suppresses migration and invasion in oral squamous cell carcinoma through inhibiting the EMT­related transcription factor SOX4.

MicroRNAs (miRs) are small, non­coding RNAs that can act as oncogenes or tumor suppressor genes in human cancer. Recent studies have revealed that miR­199a­5p is abnormally expressed in various types of human cancer; however, the potential role of miR­199a­5p in oral squamous cell carcinoma (OSCC) remains elusive. The present study investigated the role of miR­199a­5p in OSCC cells and explored the potential molecular mechanism. Reverse transcription­quantitative polymerase chain reaction was used to measure miR­199a­5p expression in OSCC tissues and adjacent normal oral epithelial tissues. Cell invasion and migration were evaluated using Transwell invasion and wound­healing assays in OSCC cells post­transfection with miR­199a­5p mimics or negative control mimics. In addition, a luciferase reporter assay was conducted to identify the target gene of miR­199a­5p in OSCC cells. The results demonstrated that miR­199a­5p expression was significantly downregulated in OSCC tissues and cell lines, and was associated with tumor progression in OSCC. Furthermore, overexpression of miR­199a­5p inhibited cell invasion and migration, and blocked the epithelial­mesenchymal transition (EMT) cascade. Notably, the results revealed that the EMT­related transcription factor SRY­box 4 (SOX4) was a direct target gene of miR­199a­5p, as determined by the direct binding of miR­199a­5p with the 3'­untranslated region of SOX4. In addition, knockdown of SOX4 by small interfering RNA­SOX4 suppressed proliferation, migration and invasion of OSCC cells. Conversely, overexpression of SOX4 rescued the suppressive effects of miR­199a­5p on cell migration and invasion. Collectively, these data indicated that miR­199a­5p may inhibit the migration and invasion of OSCC cells via targeting the EMT­related transcription factor SOX4, thus suggesting that miR­199a­5p may serve as a prognostic biomarker and therapeutic target in the treatment of OSCC.

Long non-coding RNA ENST01108 promotes carcinogenesis of glioma by acting as a molecular sponge to modulate miR-489.

Gliomas are the most common primary malignant tumor in the adult central nervous system with poor prognosis. Exploring novel biomarkers and elucidating underlying molecular mechanisms to provide effective therapeutic methods is in an urgent need. Long noncoding RNAs (lncRNAs) is involved in various human diseases including cancer. However, studies on lncRNAs and gliomas are limited. In this study, we explored the expression patterns of lncRNAs in 4 pairs of glioma samples and adjacent normal tissues via microarray and chose the most up-regulated lncRNA ENST01108 (ENST01108) to further verify its oncogenic role in glioma. Clinical data suggest that ENST01108 is closely associated with the malignant status in glioma. In vitro experiment demonstrated that overexpression of ENST01108 promoted glioma cell proliferation, migration, invasion, EMT process and survival, while knockdown of ENST01108 has an opposite effect, indicating that ENST01108 serves as an oncogenic property in glioma carcinogenesis. Further, we identified miR-489 as a direct target of ENST01108 and ENST01108 negatively regulate miR-489 by act as a sponge. SIK1 is verified as the direct target of miR-489 and it is negatively regulated by miR-489. ENST01108 also positively regulate SIKI and it promotes SIKI expression by suppressing miR-489. Taken together, the reciprocal repression of ENST011081 and miR-489 may be served as potential targets for cancer therapeutics in glioma.

LncRNA DANCR functions as a competing endogenous RNA to regulate RAB1A expression by sponging miR-634 in glioma.

Long noncoding RNA (lncRNA) differentiation antagonizing nonprotein coding RNA (DANCR) plays important regulatory roles in many solid tumors. However, the effect of DANCR in glioma progression and underlying molecular mechanisms were not entirely explored. In the present study, we determined the expression of DANCR in glioma tissues and cell lines using qRT-PCR and further defined the biological functions. Furthermore, we used luciferase reporter assay, Western blot, and RNA immunoprecipitation (RIP) to explore the underlying mechanism. Our results showed that DANCR was significantly up-regulated in glioma tissues and cell lines (U251, U118, LN229, and U87MG). High DANCR expression was correlated with advanced tumor grade. Inhibition of DANCR suppressed the glioma cells proliferation and induced cells arrested in the G0/G1 phase. In addition, we verified that DANCR could directly interact with miR-634 in glioma cells and this interaction resulted in the inhibition of downstream of RAB1A expression. The present study demonstrated that DANCR/miR-634/RAB1A axis plays crucial roles in the progression of glioma, and DANCR might potentially serve as a therapeutic target for the treatment of glioma patients.

IFI16 regulates HTLV-1 replication through promoting HTLV-1 RTI-induced innate immune responses.

Interferon (IFN)-inducible protein 16 (IFI16) regulates human immunodeficiency virus replication by inducing innate immune responses as a DNA sensor. Human T-lymphotropic virus type 1 (HTLV-1), a delta retrovirus family member, has been linked to multiple diseases. Here, we report that IFI16 expression is induced by HTLV-1 infection or HTLV-1 reverse transcription intermediate (RTI) ssDNA90 transfection. IFI16 overexpression decreases HTLV-1 protein expression, whereas IFI16 knockdown increases it. Furthermore, the knockdown of IFI16 is followed by impaired innate immune responses upon HTLV-1 infection. In addition, IFI16 forms a complex with ssDNA90 and enhances ssDNA90-triggered innate immune responses. Collectively, our data suggest a critical role for IFI16 during HTLV-1 infection by interacting with HTLV-1 RTI ssDNA90 and restricting HTLV-1 replication.

HLA-DMB restricts human T-cell leukemia virus type-1 (HTLV-1) protein expression via regulation of ATG7 acetylation.

The roles of autophagy in viral infection are complicated. While autophagy has been shown to function in host antiviral defense by eliminating intracellular viruses and regulating adaptive immunity, several viruses have evolved molecular mechanisms to get benefits from it. The deltaretrovirus human T-cell leukemia virus type-1 (HTLV-1) has been reported to profit its replication from enhancing autophagosome accumulation. Here, we reported that HLA-DMB (generally referred to here as DMB), the beta chain of the non-classical MHC-II protein HLA-DM, had strong expression in HTLV-1-transformed T-cell lines and could be induced in Hela, PMA-differentiated THP1 (PMA-THP1) or primary human monocytes by HTLV-1 infection. Immunoblot and real-time PCR assays demonstrated that overexpression of DMB decreased HTLV-1 protein expression while the knockdown of DMB increased HTLV-1 protein expression. Immunoblot and confocal microscopy assays indicated that overexpression of DMB decreased HTLV-1 induced autophagosome accumulation while the knockdown of DMB yielded the opposite effects. Coimmunoprecipitation and immunoprecipitation experiments suggested DMB interacted with autophagy-related gene (ATG) 7 and increased the acetylation of ATG7. Taken together, these results suggested DMB modulated HTLV-1 protein expression through regulation of autophagosome accumulation and our findings suggested a new mechanism by which the host cells defended against HTLV-1 infection.

miRNA-221 promotes proliferation, migration and invasion by targeting TIMP2 in renal cell carcinoma.

INTRODUCTION: MicroRNAs (miRNAs) play important roles in tumorigenesis. In this study, we investigated the role of miR-221 in the development and progression of clear cell renal cell carcinoma (ccRCC). METHODS: Quantitative real-time PCR (qRT-PCR) was used to measure the expression level of miR-221 in ccRCC tissues and cell lines. Then, we investigated the role of miR-221 to determine its potential roles on renal cancer cell proliferation, migration and invasion in vitro. A luciferase reporter assay was conducted to confirm the target gene of miR-221 and the results were validated in renal cancer cells. RESULTS: In the present study, we found that miR-221 was significantly increased in ccRCC tissues and cell lines. Knocked-down expression of miR-221 remarkably inhibited cell proliferation, migration and invasion of renal cancer cells. Moreover, at the molecular level, our results suggested that TIMP2 as a direct target of miR-221 through which miR-221 promoted tumor cell proliferation, migration and invasion. CONCLUSIONS: These findings suggested that miR-221 play an oncogenic role in the renal cancer cell proliferation, migration and invasion by directly inhibiting the tumor suppressor TIMP2, indicating miR-221 act as a potential new therapeutic target for the treatment of ccRCC.

[Clinical study on role of CD34 in patients with Biphenotypic acute leukemia].

This study was aimed to explore the expression of CD34 in patients with biphenotypic acute leukemia (BAL) and its relation with the prognosis of BAL. The flow cytometry was used to detect leukemia-associated antigen. The used monoclonal antibodys (McAb) included CD10, CD19 and CD34 for B lymphocyte lineage, CD2, CD3 and CD5 for T lymohocyte lineage, MPO, CD13 and CD33 for myeloid lineage. The finally results were respectively analyzed. The results indicated that 9 out of 216 cases of leukemia was diagnosed as BAL (4.2%). Among 9 cases of BAL, 6 cases showed the common expression of myeloid and T lymohocyte lineages (66.7%), 3 cases showed the common expression of myeloid and B lymohocyte lineages (33.3%). 4 cases of BAL displayed CD34 positive expression (44.4%). As compared with acute myelogenous leukemia (AML) and acute lymphoblastic leukemia (ALL), the BAL patients showed higher CD34 positive expression (P < 0.05). It is concluded that the BAL patients show a poor prognosis, as compared with AML or ALL patients. The therapeutic effect of BAL may negatively correlate with the CD34 positive expression.

Down-regulation of long non-coding RNA LET is associated with poor prognosis in gastric cancer.

INTRODUCTION: Long non-coding RNAs (lncRNAs) have emerged recently as major players in tumor biology and may be used for cancer diagnosis, prognosis, and potential therapeutic targets. Although down-regulation of lncRNA LET in several cancers has been studied, its role in gastric cancer remains unknown. The aim of our study was to investigate the expression, and clinical significance of lncRNA LET in gastric cancer. METHODS: The expression of lncRNA LET was detected by quantitative real-time PCR (qRT-PCR) in pairs of tumor tissues and adjacent non-tumor tissues of 93 gastric cancer patients. Then, we analyzed the potential relationship between lncRNA LET expression levels in tumor tissues and clinicopathological features of gastric cancer, and clinical outcome. RESULTS: We found that lncRNA LET expression was markedly down-regulated in tumor tissues compared with adjacent non-tumor tissues, and associated with depth of invasion, lymph node metastasis, distant metastasis, and TNM stage. Kaplan-Meier analysis showed that patients with low lncRNA LET expression had a poor overall survival than those with high lncRNA LET expression. Moreover, univariate and multivariate analyses showed that low lncRNA LET expression was an independent poor prognostic factor for gastric cancer patients. CONCLUSIONS: Our data provided the first evidence that lncRNA LET might be a novel prognostic indicator in gastric cancer and might be a potential target for diagnosis and gene therapy.

Effect of traditional Chinese medicine (Xiaochaihu Tang) on the expression of MMP-2 and MMP-9 in rats with endometriosis.

The aim of this study was to explore the effect of a traditional Chinese medicine (Xiaochaihu Tang, XCHT) on the expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 in rats with endometriosis (EMs). A total of 48 specific-pathogen-free (SPF) female Sprague-Dawley (SD) rats were randomly divided into control (n=8) and EMs (n=40) groups. The EMs model was established using a surgical procedure. At 21 days, the rats with EMs were screened and divided into four subgroups (n=8): the model control, low-dose (7.5 g/kg) XCHT-treated, high-dose (15 g/kg) XCHT-treated and gestrinone-treated (0.5 mg/kg) groups. Following 21 days of treatment, the rats were sacrificed. Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to examine the mRNA and protein levels of MMP-2 and MMP-9 in the endometrium. The expression levels of MMP-2 and MMP-9 were significantly increased in the rats with EMs compared with those in normal rats. Moreover, XCHT was able to significantly inhibit the expression of MMP-2 and MMP-9 compared with that in the model control group. In conclusion, XCHT was able to decrease the expression of MMP-2 and MMP-9 in the ectopic endometrium. The present results may provide a potential theoretical basis for the therapy of EMs.

Clinical value of a whole blood interferon-γ release assay for the diagnosis of Mycobacterium tuberculosis infection during antitubercular treatment.

The aim of this study was to evaluate the sensitivity and specificity of a whole blood interferon-γ release assay, the QuantiFERON®-TB Gold In-Tube (QFT-GIT) test, in the diagnosis of Mycobacterium tuberculosis (MTB) infection, and to assess its monitoring role during antitubercular treatment. In total, 20 patients received the QFT test, along with other commonly-used tests, prior to, and following, 2- and 6-month courses of antitubercular treatment; the results were compared and statistically analyzed. The rate of positive results for tuberculosis (TB) was 95% for the QFT test, which was significantly higher compared with those for the purified protein derivative (PPD; 55%) and the antitubercular antibody tests (15%), as well as the acid-fast bacilli smear (20%) and cultures for TB (20%; P<0.05 for all). The sensitivity and specificity of the QFT test were 96 and 93.8%, respectively. The positive result rate obtained with the QFT test was significantly higher in the TB group compared with that in the non-TB group (6.3%; P<0.05). Moreover, the positive result rate obtained with the QFT test was significantly lower in the 6-month-treated group compared with that in the 2-month group (P<0.05). In conclusion, the QFT test is a sensitive and specific method for rapidly diagnosing MTB infection, and has an improved practical clinical value in evaluating antitubercular therapies compared with that of the PPD test.