CRKL but not CRKII contributes to hemin-induced erythroid differentiation of CML.

Destruction of erythropoiesis process leads to various diseases, including thrombocytopenia, anaemia, and leukaemia. miR-429-CT10 regulation of kinase-like (CRKL) axis involved in development, progression and metastasis of cancers. However, the exact role of miR-429-CRKL axis in leukaemic cell differentiation are still unknown. The current work aimed to uncover the effect of miR-429-CRKL axis on erythropoiesis. In the present study, CRKL upregulation was negatively correlated with miR-429 downregulation in both chronic myeloid leukaemia (CML) patient and CR patient samples. Moreover, CRKL expression level was significantly decreased while miR-429 expression level was increased during the erythroid differentiation of K562 cells following hemin treatment. Functional investigations revealed that overexpression and knockdown of CRKL was remarkably effective in suppressing and promoting hemin-induced erythroid differentiation of K562 cells, whereas, miR-429 exhibited opposite effects to CRKL. Mechanistically, miR-429 regulates erythroid differentiation of K562 cells by downregulating CRKL via selectively targeting CRKL-3'-untranslated region (UTR) through Raf/MEK/ERK pathway. Conversely, CRKII had no effect on erythroid differentiation of K562 cells. Taken together, our data demonstrated that CRKL (but not CRKII) and miR-429 contribute to development, progression and erythropoiesis of CML, miR-429-CRKL axis regulates erythropoiesis of K562 cells via Raf/MEK/ERK pathway, providing novel insights into effective diagnosis and therapy for CML patients.

Network pharmacology prediction to discover the potential pharmacological action mechanism of Rhizoma Dioscoreae for liver regeneration.

Improving liver regeneration (LR) remains a medical issue, and there is currently a lack of safe and effective drugs for LR. Rhizoma Dioscoreae (SanYak, SY) is a traditional Chinese medicine. However, the underlying action mechanism of SY treatment for LR is yet to be fully elucidated. To explore the mechanism by which SY affects LR, we have conducted a series of methods for network pharmacological analysis, molecular docking, and in vivo experimental validation in mice. Overall, 9 compounds and 30 predicted target genes of SY were found to be associated with the therapeutic effects of LR. Compared with the model group, hematoxylin and eosin staining revealed that the mice with preoperative drug intervention possessed fewer postoperative hepatocyte bubbles and relatively regular morphology. Furthermore, the serum alanine transaminase and aspartate aminotransferase levels were reduced, immunohistochemistry revealed elevated proliferating cell nuclear antigen positivity rate, and Western blotting demonstrated that the phospho-protein kinase B (AKT)/AKT ratio was downregulated and that vascular endothelial growth factor A (VEGFA) expression levels were upregulated. This study explored dioscin, the main active ingredient of SY, and its potential therapeutic effects on LR. It repairs damaged liver following surgery and promotes liver cell proliferation. The action mechanism comprises reducing AKT phosphorylation levels and upregulating VEGFA expression levels. Thus, this study provides a new direction for further research on the mechanism of SY promoting LR.

Butyrate ameliorates colorectal cancer through regulating intestinal microecological disorders.

The occurrence and progression of colorectal cancer (CRC) are closely related to intestinal microecological disorders. Butyrate, the representative of short chain fatty acids, possess anti-inflammatory and antioxidant effects, and its antitumor effect has been gradually paid attention to. In this study, azoxymethane/dextran sodium sulfate induced mouse CRC model was used to explore the role and mechanism of butyrate in regulating colon cancer and its intestinal microecological balance. Outcomes exhibited that butyrate alleviated weight loss, disease activity index, and survival in CRC mice and inhibited tumor number and progression. Further research revealed that butyrate restrained the aggregation of harmful while promoting the colonization of beneficial flora, such as Actinobacteriota, Bifidobacteriales and Muribaculacea through 16S rDNA sequence analysis. This study confirmed that butyrate can ameliorate CRC by repairing intestinal microecology, providing ideas and evidence for chemical prophylactic agents, such as butyrate to remedy tumors and regulate tumor microbiota.

ETV6 Regulates Hemin-Induced Erythroid Differentiation of K562 Cells through Mediating the Raf/MEK/ERK Pathway.

As a member of transcription factor E-Twenty Six (ETS) family, ETS variant 6 (ETV6) plays significant role in hematopoiesis and embryonic development. ETV6 dysexpression also involved in the occurrence, development and progression of cancers and leukemia. In current work, we hypothesized that ETV6 plays a role in erythroid differentiation of chronic myeloid leukemia (CML). We found the protein expression level of ETV6 was significantly upregulated during hemin-induced erythroid differentiation of K562 cells. Moreover, overexpression of ETV6 inhibited erythroid differentiation in hemin-induced K562 cells with decreased numbers of benzidine-positive cells and decreased expression levels of erythroid differentiation specific markers glycophorin (GPA), CD71, hemoglobin A (HBA), α-globin, γ-globin and ε-globin. Conversely, ETV6 knockdown promoted erythroid differentiation in hemin-induced K562 cells. Furthermore, ETV6 expression level slightly positively with the proliferation capacity of K562 cells treated with hemin. Mechanistically, ETV6 overexpression inhibited fibrosarcoma/mitogen activated extracellular signal-regulated kinase/extracellular regulated protein kinase (Raf/MEK/ERK) pathway, ETV6 knockdown activated the Raf/MEK/ERK pathway. Collectively, the current work demonstrates that ETV6 plays an inhibitory role in the regulation of K562 cell erythroid differentiation via Raf/MEK/ERK pathway, it would be a potentially therapeutic target for dyserythropoiesis.

Complete mitochondrial genomes of Thyreophagus entomophagus and Acarus siro (Sarcoptiformes: Astigmatina) provide insight into mitogenome features, evolution, and phylogeny among Acaroidea mites.

Mites from the Acaroidea (Sarcoptiformes: Astigmatina) are important pests of various stored products, posing potential threats to preserved foods. In addition, mites can cause allergic diseases. Complete mitochondrial genomes (mitogenomes) are valuable resources for different research fields, including comparative genomics, molecular evolutionary analysis, and phylogenetic inference. We sequenced and annotated the complete mitogenomes of Thyreophagus entomophagus and Acarus siro. A comparative analysis was made between mitogenomic sequences from 10 species representing nine genera within Acaroidea. The mitogenomes of T. entomophagus and A. siro contained 37 genes, including 13 protein-coding genes (PCGs), 22 transfer RNAs (tRNAs), two ribosomal RNAs (rRNAs), and one control region. In Acaroidea species, mitogenomes have highly conserved gene size and order, and codon usage. Among Acaroidea mites, most PCGs were found to be under purifying selection, implying that most PCGs might have evolved slowly. Our findings showed that nad4 evolved most rapidly, whereas cox1 and cox3 evolved most slowly. The evolutionary rates of Acaroidea vary considerably across families. In addition, selection analyses were also performed in 23 astigmatid mite species, and the evolutionary rate of the same genes in different superfamilies exhibited large differences. Phylogenetic results are mostly consistent with those identified by previous phylogenetic studies on astigmatid mites. The monophyly of Acaroidea was rejected, and the Suidasiidae and Lardoglyphidae appeared to deviate from the Acaroidea branch. Our research proposed a review of the current Acaroidea classification system.

CRKL promotes hepatocarcinoma through enhancing glucose metabolism of cancer cells via activating PI3K/Akt.

Abnormal glucose metabolism may contribute to cancer progression. As a member of the CRK (v-crk sarcoma virus CT10 oncogene homologue) adapter protein family, CRKL (CRK-like) associated with the development and progression of various tumours. However, the exact role and underlying mechanism of CRKL on energy metabolism remain unknown. In this study, we investigated the effect of CRKL on glucose metabolism of hepatocarcinoma cells. CRKL and PI3K were found to be overexpressed in both hepatocarcinoma cells and tissues; meanwhile, CRKL up-regulation was positively correlated with PI3K up-regulation. Functional investigations revealed that CRKL overexpression promoted glucose uptake, lactate production and glycogen synthesis of hepatocarcinoma cells by up-regulating glucose transporters 1 (GLUT1), hexokinase II (HKII) expression and down-regulating glycogen synthase kinase 3ß (GSK3ß) expression. Mechanistically, CRKL promoted glucose metabolism of hepatocarcinoma cells via enhancing the CRKL-PI3K/Akt-GLUT1/HKII-glucose uptake, CRKL-PI3K/Akt-HKII-glucose-lactate production and CRKL-PI3K/Akt-Gsk3ß-glycogen synthesis. We demonstrate CRKL facilitates HCC malignancy via enhancing glucose uptake, lactate production and glycogen synthesis through PI3K/Akt pathway. It provides interesting fundamental clues to CRKL-related carcinogenesis through glucose metabolism and offers novel therapeutic strategies for hepatocarcinoma.

Disruption of Fis reduces bacterial persister formation by regulating glutamate metabolism in Salmonella.

The presence of persisters causes recalcitrance to antibiotic treatment, and can be attributed to a fairly large number of clinically refractory infections in several species of bacteria. Many studies have explored this phenomenon, but the mechanisms remain poorly understood. In this study, we found that the deletion of fis, which encodes a key DNA-binding protein mediating various biological processes, significantly reduced persister formation in S. Typhi. Persister assays and glutamate determination analysis showed that Fis mediated Salmonella persistence through regulating glutamate metabolism. Additionally, glutamate incubation altered the expression of the stringent response regulatory genes, demonstrating that the stringent response was related to glutamate regulation by Fis. The findings revealed that glutamate metabolism regulated by Fis serves as a mechanism for persister formation in S. Typhi.

Fabrication of cerium doped carbon dots with highly radical scavenging activity alleviates ferroptosis-induced oxidative damage.

Ferroptosis as an iron-dependent lipid peroxidation process causes sevely oxidative damage of cell, but lack of highly efficient and recycable antioxidant agents. To this end, cerium doped carbon dots (Ce-doped CDs) with radical scavenging activity were synthesized using a simple microwave-assisted hydrothermal carbonization. The resultant Ce-doped CDs exhibited an ultra-small size of only approximately 2.6 nm, excellent dispersion in water as well as optical performance. Taking advantage of inherent ultra-small size, Ce-doped CDs were endowed with high Ce3+/Ce4+ratio, which significantly enhanced their radical scavenging activity. Meanwhile, the Ce-doped CDs with superior biocompatibility could enter cells quickly and then localized in the cytoplasm. As we expected, the Ce-doped CDs strongly protected cells from oxidative damage of erastin-mediated ferroptosis. These findings suggest that the as-prepared Ce-doped CDs have the potential to be antioxidant drugs against for ferroptosis-induced oxidative damage.

The potential role of miR-124-3p in tumorigenesis and other related diseases.

MicroRNAs (miRNAs) are a class of single-stranded noncoding and endogenous RNA molecules with a length of 18-25 nucleotides. Previous work has shown that miR-124-3p leads to malignant progression of cancer including cell apoptosis, migration, invasion, drug resistance, and also recovers neural function, affects adipogenic differentiation, facilitates wound healing through control of various target genes. miR-124-3p has been mainly previously characterized as a tumor suppressor regulating tumorigenesis and progression in several cancers, such as hepatocellular carcinoma (HCC), gastric cancer (GC), bladder cancer, ovarian cancer (OC), and leukemia, as a tumor promotor in breast cancer (BC), and it has been also widely studied in a variety of neurological diseases, like Parkinson's disease (PD), dementia and Alzheimer's disease (AD), and cardiovascular diseases, ulcerative colitis (UC), acute respiratory distress syndrome (ARDS). To lay the groundwork for future therapeutic strategies, in this review we mainly focus on the most recent years of literature on the functions of miR-124-3p in related major cancers, as well as its downstream target genes. Although current work as yet provides an incomplete picture, miR-124-3p is still worthy of more attention as a practical and effective clinical biomarker.

One-pot synthesis of cerium and praseodymium co-doped carbon quantum dots as enhanced antioxidant for hydroxyl radical scavenging.

The antioxidant activity of ceria nanoparticles is tightly regulated by size distribution and heteroatom doping. Inspired by this rule, cerium and praseodymium codoped carbon quantum dots (Ce/Pr-CQDs) were synthesized through the one-pot hydrothermal carbonization method. Taking intrinsic advantage of CQDs, the resultant Ce/Pr-CQDs exhibited uniform and ultra-small morphology with an average size of 2.8 nm, which led to an increased proportion of Ce3+. In addition, the doping of Pr into Ce-CQDs improved the redox properties. As we expected, the Ce/Pr-CQDs possessed enhanced hydroxyl radical scavenging properties compared with the cerium-doped carbon quantum dots (Ce-CQDs). Furthermore, Ce/Pr-CQDs with favorable biocompatibility and negligible cytotoxicity are readily internalized into cytoplasm, decreasing the level of reactive oxygen species (ROS). Taken together, the resultant Ce/Pr-CQDs displayed great potential for applications relating to oxidative-stress-associated disease.

Platelet indices in patients with chronic inflammatory arthritis: a systematic review and meta-analysis.

Correlation between platelet indices and chronic inflammatory arthritis (CIA) remains a moot point today. This meta-analysis aimed to evaluate whether platelet (PLT) count, mean platelet volume (MPV) and platelet distribution width (PDW) associated with rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA). A systematic literature search was performed in PubMed, EMBASE, and Web of Science up to August 2019. Pooled standardized mean differences (SMD) and 95% confidence interval (CI) were calculated using a random-effect model. As a result, 34 studies were included, encompassing 17 on RA, 12 on AS, 3 on PsA and 2 on both RA and AS. In these studies, PLT count was significantly higher in RA (SMD = 0.55, 95% CI = 0.36-0.73, P < .001), AS (SMD = 0.53, 95% CI = 0.36-0.70, P < .001) and PsA patients (SMD = 1.29, 95% CI = 0.82-1.77, P < .001) than that in healthy subjects, while MPV and PDW presented nonsignificant differences in these intergroup comparisons (P > .05), and similar results were observed in subgroup analyses. The meta-regression analysis demonstrated that there were strong positive correlations between erythrocyte sedimentation rate and PLT count, and weak correlation trend between the disease activity score and PLT count in both RA and AS subjects without statistically significant difference. The sensitivity analysis indicated that these results were not unduly influenced by any single study. In conclusion, this meta-analysis demonstrated that PLT count was elevated in CIA patients and could be suitable for evaluating the disease activity, whereas MPV and PDW were independent of CIA.

Fetuin-a to adiponectin ratio is a sensitive indicator for evaluating metabolic syndrome in the elderly.

BACKGROUND: Fetuin-A and adiponectin present significant associations, supported by recent evidence, with metabolic syndrome (MS) featuring hyperglycemia, central obesity and insulin resistance as the main components, but their biological functions are opposite. The aim of this study was to verify whether fetuin-A/adiponectin ratio (F/A ratio) is a more sensitive indicator for evaluation of MS than either fetuin-A or adiponectin. METHODS: In this cross-sectional study, 465 elderly subjects were selected from the physical examination database. Serum levels of fetuin-A and adiponectin were measured using an enzyme-linked immunosorbent assay (ELISA) method. Spearman's rank correlation coefficient, linear regression and logistic regression analysis were adopted to estimate the correlations of fetuin-A, adiponectin and F/A ratio with MS and its components, and receiver operating characteristic (ROC) curve analysis was performed to evaluate the predictive values of the aforesaid indices. RESULTS: Compared with fetuin-A or adiponectin, F/A ratio was significantly associated with all the components of MS, and this correlation was significant even after adjusting potential confounding factors (P < 0.05). Logistic regression analysis indicated that F/A ratio presented a stronger correlation with incident MS (adjusted OR: 1.466; 95% CI: 1.189-1.808) than fetuin-A (adjusted OR: 1.100; 95% CI: 1.020-1.186) and adiponectin (adjusted OR: 0.760; 95% CI: 0.664-0.871) alone. ROC analysis revealed that F/A ratio achieved a larger area under curve (AUC) than fetuin-A and adiponectin, with their AUC values of 0.755, 0.709 and 0.708, respectively. CONCLUSION: F/A ratio is a more sensitive index for evaluating MS than either fetuin-A or adiponectin in the elderly.

Spaghetti, a homolog of human RPAP3 (RNA polymerase II-associated protein 3), determines the fate of germline stem cells in Drosophila ovary.

The Drosophila ovary provides an attractive model for studying the extrinsic or intrinsic factors that regulate the fate of germline stem cells (GSCs). Using this model, we identified a new role for Drosophila spaghetti (spag), encoding a homolog of human RNA polymerase II-associated protein 3 (RPAP3), in regulating the fate of ovarian GSCs. Results from spag knockdown and genetic mosaic studies suggest that spag functions as an intrinsic factor for GSCs maintenance. Loss of Spag by, either spag RNAi or null mutation failed to trigger apoptosis in ovarian GSCs. Overexpression of spag led to negligible increases in the number of GSC/Cystoblast (CB) cells, suggesting that an excess of Spag is not sufficient to accelerate the proliferation of GSCs or delay CBs' differentiation. Our study provides evidence supporting that spag is involved in adult stem cells maintenance. In addition, the RNAi screen results showed that knockdown of Hsp90, one of known Spag interacting partners, led to loss of ovarian GSCs in Drosophila. Heterozygous mutations in hsp90 (hsp90/+) dramatically accelerated the GSC loss in spag RNAi ovaries, suggesting that the Spag-contained complex possibly plays an essential role in controlling the GSCs fate.

Circulating chemerin levels and gestational diabetes mellitus: a systematic review and meta-analysis.

BACKGROUND: Chemerin is a novel adipokine which is associated with metabolic syndrome and type 2 diabetes mellitus. However, recent investigations regarding circulating chemerin levels in gestational diabetes mellitus (GDM) are conflicting. This meta-analysis is to evaluate and determine their associations. METHODS: A systematic literature search was performed in PubMed, EMBASE and Web of Science up to 13 December 2017. Pooled standardized mean differences (SMD) and 95% confidence interval (CI) were calculated using a random-effect model. RESULTS: Eleven studies comprising 742 GDM patients and 840 normal pregnant women were included. Circulating chemerin levels were increased in GDM patients compared with healthy pregnant women (SMD: 1.16; 95% CI: 0.29, 2.04; P = 0.009). Subgroup analyses revealed such difference was especially available in the groups of the second trimester (SMD: 1.47; 95% CI: 0.28, 2.67) and mean age < 30 years (SMD: 2.30; 95% CI: 0.69, 3.91) of GDM patients. There was significant heterogeneity among studies (I2 = 98.0%, P < 0.001); however, heterogeneity disappeared or markedly decreased in the subgroups of European populations (I2 = 0.0%, P = 0.531), age ≥ 30 years (I2 = 28.2%, P = 0.223) and WHO diagnostic criteria (I2 = 0.0%, P = 0.490) when stratifying by study location, trimester of chemerin measurement and the diagnostic criteria of GDM. CONCLUSIONS: The elevated levels of circulating chemerin were associated with GDM, which suggests it might play an important role in the pathogenetic mechanism of GDM.

Cyclin B3 Deficiency Impairs Germline Stem Cell Maintenance and Its Overexpression Delays Cystoblast Differentiation in Drosophila Ovary.

It is well known that cyclinB3 (cycB3) plays a key role in the control of cell cycle progression. However, whether cycB3 is involved in stem cell fate determination remains unknown. The Drosophila ovary provides an exclusive model for studying the intrinsic and extrinsic factors that modulate the fate of germline stem cells (GSCs). Here, using this model, we show that DrosophilacycB3 plays a new role in controlling the fate of germline stem cells (GSC). Results from cycB3 genetic analyses demonstrate that cycB3 is intrinsically required for GSC maintenance. Results from green fluorescent protein (GFP)-transgene reporter assays show that cycB3 is not involved in Dad-mediated regulation of Bmp signaling, or required for dpp-induced bam transcriptional silencing. Double mutants of bam and cycB3 phenocopied bam single mutants, suggesting that cycB3 functions in a bam-dependent manner in GSCs. Deficiency of cycB3 fails to cause apoptosis in GSCs or influence cystoblast (CB) differentiation into oocytes. Furthermore, overexpression of cycB3 dramatically increases the CB number in Drosophila ovaries, suggesting that an excess of cycB3 function delays CB differentiation. Given that the cycB3 gene is evolutionarily conserved, from insects to humans, cycB3 may also be involved in controlling the fate of GSCs in humans.

Circulating retinol binding protein 4 levels in nonalcoholic fatty liver disease: a systematic review and meta-analysis.

BACKGROUND: Retinol binding protein 4 (RBP4) is implicated in obesity, insulin resistance and type 2 diabetes mellitus that are closely associated with nonalcoholic fatty liver disease (NAFLD). However, recent investigations regarding circulating RBP4 levels in NAFLD are conflicting. This meta-analysis is to determine whether NAFLD, non-alcoholic steatohepatitis (NASH) and simple steatosis (SS) patients have altered RBP4 levels. METHODS: We performed a systematic search in PubMed, EMBASE and The Cochrane Library up until 18 March 2017, and 12 studies comprising a total of 4247 participants (2271 NAFLD patients and 1976 controls) were included in the meta-analysis. RESULTS: There were no significant differences of circulating RBP4 levels in the following comparisons: (1) NAFLD patients vs controls (standardized mean differences [SMD]: 0.08; 95% CI: -0.21, 0.38); (2) NASH patients vs controls (SMD: -0.49; 95% CI: -1.09, 0.12); (3) SS patients vs controls (SMD: -0.72; 95% CI: -1.64, 0.20) and (4) NASH vs SS patients (SMD: -0.04; 95% CI: -0.32, 0.24). The results remained essentially unchanged in the comparisons between NAFLD patients and controls after excluding single individual study or bariatric studies (n = 2). No significant publication bias was detected. However, there was significant heterogeneity among studies and the subgroup and meta-regression analyses did not find the potential sources. CONCLUSIONS: Circulating RBP4 levels may not be associated with NAFLD. Further prospective cohort studies are required to confirm these findings.

ANXA5 level is linked to in vitro and in vivo tumor malignancy and lymphatic metastasis of murine hepatocarcinoma cell.

AIM: To investigate ANXA5 overexpression on in vitro and in vivo malignancies of murine Hca-P cells. MATERIALS & METHODS: Hca-P with low lymph node metastasis (LNM) potential was used as cell model. TEM, CCK-8 and Boyden transwell assays were performed for in vitro Hca-P behaviors. Hca-P-transplanted mouse model was established for in vivo experiment. RESULTS: ANXA5-overexpressing monoclonal Anxa5-Hca-P-1, Anxa5-Hca-P-2 and Anxa5-Hca-P-3 cells were obtained. ANXA5 upregulation alters the proliferation, morphology and rough endoplasmic reticulum of Hca-P cells, enhances in vitro migration and invasions of Hca-P, promotes in vivo malignant degree and LNM rate of Anxa5-Hca-P-3-transplanted mice. CONCLUSION: As a potential indicator for malignancy and lymphatic metastasis, ANXA5 overexpression increases in vitro migration and invasion of Hca-P cell, promotes in vivo malignancy, LNM rate and level of Hca-P-transplanted mice.

Elevated GAPDH expression is associated with the proliferation and invasion of lung and esophageal squamous cell carcinomas.

Glyceraldehyde-3-phosphate dehydrogenase, is one of the most investigated housekeeping genes and widely used as an internal control in analysis of gene expression levels. The present study was designed to assess whether GAPDH is associated with cancer cell growth and progression and, therefore may not be a good internal control in cancer research. Our results from clinical tissue studies showed that the levels of GAPDH protein were significantly up-regulated in lung squamous cell carcinoma tissues, compared with the adjacent normal lung tissues, and this was confirmed by western blotting and immunohistochemistry. GAPDH knockdown by siRNA resulted in significant reductions in proliferation, migration, and invasion of lung squamous carcinoma cells in vitro. In a nude mouse cancer xenograft model, GAPDH knockdown significantly inhibited the cell proliferation and migration/invasion in vivo. In summary, GAPDH may not be an appropriate internal control for gene expression studies, especially in cancer research. The role of GAPDH in cancer development and progression should be further examined in pre-clinical and clinical studies.

Serum fetuin-A concentrations are positively associated with serum VEGF levels in patients with newly diagnosed type 2 diabetes.

Fetuin-A was considered to be involved in pathogenesis of type 2 diabetes. On the other hand, higher vascular endothelial growth factor (VEGF) expression is associated with diabetes and its vascular complications, but the mechanisms leading to higher VEGF levels are still not clear. To the best of our knowledge, there are no data to show the associations between fetuin-A and VEGF in patients with type 2 diabetes. Therefore, the aim of this study is to investigate the relationship between serum fetuin-A concentrations and serum VEGF levels in patients with type 2 diabetes. We recruited 345 patients with newly diagnosed type 2 diabetes. Serum fetuin-A concentrations and serum VEGF levels were measured using enzyme-linked immunosorbent assay (ELISA) method. In this study, there was a significant positive correlation between serum fetuin-A concentrations and serum VEGF levels (r=0.223, P<0.001), and the correlation remained significant even after adjustment for other confounding factors in the multivariate regression model (ß=0.151, P=0.006). Mantel-Haenszel (M-H) stratified analysis showed that the degree of association of high concentrations of fetuin-A with high levels of VEGF is higher than that with low levels of VEGF (odds ratio of M-H [ORM-H], 2.938; 95% confidence interval [CI], 1.896-4.553). In addition, this study showed that both fetuin-A and VEGF were positively associated with fasting plasma glucose (FPG), glycated hemoglobin A1c (HbA1c) and C-reactive protein (CRP). These data suggested that serum fetuin-A concentrations were positively associated with serum VEGF levels in patients with newly diagnosed type 2 diabetes.

The role of CT10 regulation of kinase-like in cancer.

V-crk avian sarcoma virus CT10 oncogene homolog-like (CRKL) is a member of CRK family. It acts as an adaptor protein in intracellular signal transduction. CRKL has been reported overexpressed in a variety of cancers affecting the aggressive and malignant behaviors of cancer cells. CRKL seems to show a tumor-promotion role in gastric cancer, glioblastoma multiforme, hepatocellular carcinoma, bladder cancer, lung cancer, colon cancer, ovarian cancer, leukemia, breast cancer, head and neck cancer, rhabdomyosarcoma and neuroblastoma. The association of CRKL with malignant tumors and its potential action mechanisms were summarized. CRKL has the potential to be used as a biomarker for the diagnosis, treatment and prognosis of certain tumors.