Silencing CDC25A or treatment with CDC25A inhibitor could reverse the B7-H3-induced chemoresistance of cancer cells. Moreover, both B7-H3 and CDC25A were significantly upregulated in CRC samples compared with normal adjacent tissues and that the levels correlated with tumor stage. CDC25A was positively correlated with B7-H3 expression in this cohort. Taken together, our findings provide an alternative mechanism by which CRC cells can acquire chemoresistance via the B7-H3/CDC25A axis. © The author(s).The aim of this study was to explore and identify the key genes and signal pathways contributing to cervical intraepithelial neoplasia (CIN). The gene expression profiles of GSE63514 were downloaded from Gene Expression Omnibus database. Differentially expressed genes (DEGs) were screened performing with packages in software R. After Gene ontology terms, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyzing, and Gene set enrichment analysis (GSEA), weighted gene co-expression network analysis (WGCNA) was used to analyze these genes. Then sub-modules were subsequently analyzed base CIN grade, and protein-protein interaction (PPI) network of DEGs were constructed. 537 DEGs were screened in total, consisting 331 up-regulated genes and 206 down-regulated genes in CIN samples compared to normal samples. The most DEGs were enriched in chromosomal region in cellular component (CC), organelle fission inbiological process (BP) and ATPase activity in molecular function (MF). KEGG pathway enrichment analyzing found the DEGs were mainly concentrated in 10 pathways. The results of GSEA mainly enriched in 4 functional sets E2F-Targets, G2M-Checkpoint, Mitotic-Spindle and Spermatogenesis. A total of 6 modules were identified by WCGNA. Subsequently, grey module was the highest correlation (Cor=0.78, P=5e-22) and 31 genes were taken as candidate hub genes for CIN high grade risk (weighted correlation coefficients >0.80). Finally, diagnostic analysis showed that in addition to CCDC7, the expression levels of the remaining 13 DEGs have a high diagnostic value (AUC>0.8 and P less then 0.05). These findings provided a new sight into the understanding of molecular functions for CIN. © The author(s).Background Colorectal cancer (CRC) is one of the most common malignant tumors in the world. Lymph node metastasis (LNM) is a common mode of metastasis of CRC. However, the combined mRNA biomarkers associated with LNM of CRC that can effectively predict CRC prognosis have not been reported yet. Methods To identify biomarkers that are associated with LNM, we collected data from the The Cancer Genome Atlas (TCGA) database. The edgeR package was searched to seek LNM-related genes by comparisons between cancer samples and normal colorectal tissues and between LNM and non-LNM (NLNM) of CRC. Univariate and multivariate regression analysis of genes in the intersection to build gene signature associated with independent prognosis of CRC, and then verified by Kaplan-Meier curve and log-rank test, receiver operating characteristic (ROC) curve was used to determine the efficiency of survival prediction of our four-mRNA signature. Finally, the potential molecular mechanisms and properties of these gene signature were also biosynthesis. Conclusions By conducting TCGA data mining, our study demonstrated that a four-mRNA signature associated with LNM can be used as a combined biomarker for independent prognosis of CRC. © The author(s).Cervical cancer is a commonly diagnosed cancer among females. Polymorphisms in pre-microRNAs have been demonstrated to play critical roles in cancer. However, the roles of pre-microRNA polymorphisms in the aetiology of cervical cancer have not been well documented. We genotyped eight pre-microRNA polymorphisms in 290 cervical cancer patients and 445 cancer-free female controls using quantitative polymerase chain reaction with TaqMan probes. To estimate the association between pre-microRNA polymorphisms and the risk of cervical cancer, an unconditional logistic regression model was used to calculate the odds ratio (OR) and 95% confidence interval (CI), adjusting for age, menopause, delivery, and abortion. We found that the pre-miR-137 rs1625579 T > G polymorphism was associated with a significant decrease in cervical cancer risk (TG/GG versus TT adjusted OR (AOR) = 0.47, 95% CI = 0.27-0.81; TG versus TT AOR = 0.56, 95% CI = 0.34-0.91). We also observed a significant association between the pre-miR-27a rs895819 T > C polymorphism and decreased cervical cancer risk (TC/CC versus TT AOR = 0.65, 95% CI = 0.44-0.96). Stratified analysis further demonstrated that the pre-miR-137 rs1625579 T > C and pre-miR-27a rs895819 T > C polymorphisms significantly reduced the risk of cervical cancer susceptibility in patients younger than 49 years, those who experienced fewer abortions, and clinical stage I patients. Moreover, the pre-miR-137 rs1625579 T > G polymorphism showed protective effects in premenopausal women, squamous cell carcinoma patients, and patients with unclassified types of pathologies; the pre-miR-27a rs895819 T > C polymorphism was also associated with a decreased risk in patients older than 49 years, menopausal women, and women who had experienced vaginal pregnancies. The pre-miR-137 rs1625579 T > G and pre-miR-27a rs895819 T > C polymorphisms may provide protective effects against susceptibility to cervical cancer risk. © The author(s).Background Apigenin, a flavonoid phytochemical extracted from fruits and vegetables, has shown anti-neoplastic effects in a variety of malignant tumors.  https://www.selleckchem.com/products/itacnosertib.html  DLBCL is the most common type of aggressive lymphoma in adults with a poor prognosis. Small-molecule inhibitors like BTK inhibitors have demonstrated extended period of disease control. Whereas the effects of the synergetic inhibition of the two have not been elucidated. Methods We assessed the efficacy of Apigenin alone or combined with Abivertinib to inhibit DLBCL progression. Cell viability was examined using the cell proliferation cell proliferation assay (MTS). Apoptotic cells and cell cycle evaluation were detected by Annexin V-FITC and DNA staining solution respectively. Western blot was used to explore the potential mechanism, and the in vivo effects of the two drugs were performed by a DLBCL xenograft BALB/c nude mice model. Results Our results demonstrated that Apigenin can inhibit the proliferation and clone forming of DLBCL cells. Apigenin also induces apoptosis by down-regulating BCL-XL and activating Caspase family.