GSEA showed that some metabolism-related pathways were associated with the high CDK5 expression phenotype. In vitro experiments showed that CDK5 knockdown impaired cell proliferation and colony formation ability, and induced apoptosis and cell cycle arrest. Conclusion CDK5 may act as a potential biomarker of glioma progression and a valid target for glioma therapy.MicroRNAs (miRNAs) are small, noncoding RNAs which can bind to target mRNAs and regulate gene expression. Increasing evidences suggest that miRNAs play an important role in driving hepatocellular carcinoma (HCC) progression by regulating tumor cell proliferation, apoptosis, invasion, and migration. In this study, we demonstrated that the expression of microRNA-30a-3p (miR-30a-3p) was reduced in HCC cell lines in comparison to immortalized liver cell line, LO2. Augmented miR-30a-3p level markedly inhibited MHCC-97H cell growth, migration and invasion in vitro. MiR-30a-3p was also found to inhibit tumor growth in vivo using tumor-bearing mice. Mechanismly, COX-2 was discovered to be a direct and functional target of miR-30a-3p in MHCC-97H cells. Raised miR-30a-3p expression reduced the transcriptional level of COX-2 in MHCC-97H cells, while genetically upregulated COX-2 expression was able to reverse the function of miR-30a-3p-mediated suppression of MHCC-97H cells growth, migration and invasion. In addition, we found that using a COX-2 inhibitor, celecoxib, could enhance the anti-metastatic role of miR-30a-3p in MHCC-97H cells. Lastly, we found that decreased COX-2 protein level affected PGE2 production, leading to lower Bcl-2, Caspase-3, MMP2 and MMP9 expression but higher Bax and E-cadherin expression, which in turn culminated in higher rates of cell death and lower rates of cell migration. Taken together, our findings demonstrate that miR-30a-3p could be a target for the treatment of hepatocellular carcinoma cells progression.Esophageal Squamous Cell Carcinoma (ESCC) is the predominant type of Esophageal Cancer (EC), accounting for nearly 88% of EC incidents worldwide. https://www.selleckchem.com/products/azd9291.html Importantly, it is also a life-threatening cancer for patients diagnosed in advanced stages, with only a 20% 5-year survival rate due to a limited number of actionable targets and therapeutic options. Increasing evidence has shown that inter-tumor and intra-tumor heterogeneity are widely distributed across ESCC tumor tissues. In our work, multi-omics data from ESCC cell lines, tumor tissue, normal tissue and Patient-Derived Xenograft (PDX) tissues were analyzed to investigate the heterogeneity among ESCC samples at the DNA, RNA, and protein level. We identified enrichment of ECM-receptor interaction and Focal adhesion pathways from the subset of protein-coding genes with non-silent mutations in ESCC patients. We also found that TP53, TTN, KMT2D, CSMD3, DNAH5, MUC16 and DST are the most frequently mutated genes in ESCC patient samples. Out of the identified genes, TPbserved trans-species heterogeneity in as high as 75% of the identified proteins, indicating that the ambiguity of proteins should be addressed by specific strategies to avoid drawing false conclusions. The identification and characterization of gene mutation and expression heterogeneity across different ESCC datasets, including various novel TP53 mutations, ECM-receptor interaction, Focal adhesion, and Olfactory transduction pathways (CNGB1), provide researchers with evidence and implications for accurate research and precision therapeutic development.Aim Although there are so many treatment strategies used for hepatocellular carcinoma (HCC), the overall survival (OS) of HCC patients still remains very low. In our previous studies, asparagus polysaccharide (ASP) has been demonstrated to suppress proliferation, migration, invasion and angiogenesis of HCC cells under normoxic conditions in vitro. However, the inhibitory effects of ASP on the hypoxia-induced migration, invasion and angiogenesis of HCC cells still remain largely unexplored. Materials and methods Cell Counting Kit-8 (CCK-8) assay, transwell assay, and tube formation assay were used to determine the effects of ASP on hypoxia-induced proliferation, migration, invasion and angiogenesis of HCC cells. ELISA, Western blotting analysis and immunofluorescence assay were used to confirm the effects of ASP on the expressions of HIF-1α and VEGF at the protein level. Moreover, effects of ASP on signaling pathway-related proteins were investigated by Western blotting analysis. Immunohistochemistry (IHC) ass/VEGF expression via MAPK and PI3K signaling pathways.Background At the time of diagnosis, colorectal cancer (CRC) patients are usually in an advanced stage of disease, which is accompanied by metastasis. Long noncoding RNAs (lncRNAs) play critical regulatory roles in cancer biology. However, the contributions of lncRNA LINC01272 to CRC remain elusive. Methods Bioinformatics and the survminer R package were used to predict intermolecular correlations and prognostic indicators. Quantitative real-time PCR was used to examine molecular expression. In vitro experiments, including migration assays, invasion assays, and wound healing assays, were used to investigate the effects of LINC01272, ITGB2 and miR-876 on CRC cell migration and invasion abilities. Furthermore, a dual-luciferase reporter gene assay was performed to explore the potential mechanism by which LINC01272 contributes to CRC. Results We found that LINC01272 was highly expressed in multiple cancers and closely related to core epithelial-mesenchymal transition (EMT) factors and that high levels of LINC01272 are associated with a poor prognosis in CRC patients. qRT-PCR revealed that LINC01272 was highly expressed and negatively associated with miR-876 in CRC. Additionally, LINC01272 or ITGB2 silencing reduced, while miR-876 overexpression promoted, the invasiveness and metastatic capacity of CRC cells in vitro. Moreover, LINC01272 potentially targeted miR-876, and miR-876 potentially targeted ITGB2. Conclusion LINC01272 was highly expressed in CRC and predicted a poor prognosis. LINC01272 promoted EMT and metastasis by regulating miR-876/ITGB2 to act as an oncogene in CRC. LINC01272 may be a promising prognostic biomarker and therapeutic target for the treatment of CRC patients in the future.