RESUMO
Objective To investigate the expression and significance of the adaptor protein epsin 3 (EPN3) in colorectal cancer in order to provide reference for further stud)' of EPN3. Methods GEPIA and GEDS were used to analyze the expression of EPN3 in colorectal cancer tissues and cells. SMART and cBioPortal databases were used to analyze the relationship between EPN3 gene metfrylation and cop)' number variation and its expression level. Metascape was used to complete analysis of gene ontology functional annotation and related pathways of EPN3 related genes and BioPlex was applied to construct a protein network in HCT116 cell. Thirteen pairs of colorectal cancer adjacent tissue and cancer tissue specimens were collected, and EPN3 mRNA expression were detected by Real-time PCR. The effect of abilities of cell proliferation, clone formation and migration via silencing EPN3 in HCT116 and HT29 were observed. Results GEPIA, GEDS, SMART and cBioPortal analyses showed that EPN3 was highly expressed in colorectal tumor tissues (P<0. 01), and was related to methylation and copy number variation. The enrichment result of EPN3 related genes showed that it was mainly related to cell adhesion. And a protein interaction network constructed by CCDC130, TNFAIP1, PHGDH, EPN2, etc. was related to protein ubiquitination. Real-time PCR result showed that EPN3 was highly expressed in tumor tissues (P<0. 05). Silencing EPN3 inhibited the proliferation, clony formation and migration abilities of HCT116 and HT29 cells. Conclusion EPN3 is highly expressed in colorectal cancer tissues and is related to cell adhesion and protein ubiquitination. Down-regulated EPN3 can inhibit abilities of proliferation, clony formation and migration of HCT116 and HT29 cells, and this could provide a reference for further research on EPN3.
RESUMO
Objective To observe the expression of pleckstrin homology like domain family A member 2 (PHLDA2) in hepatocellular carcinoma (HCC) and investigate the effects of PHLDA2 on cell proliferation, migration, invasion and apoptosis. Methods To analyze the expression of PHLDA2 in 369 cases of HCC tissues and 160 cases of adjacent normal tissues and the effect of PHLDA2 expression on overall survival rate of HCC patients by gene expression profiling interactive analysis (GEPIA) online database. Cell proliferation was determined by cell counting kit-8 (CCK-8) and colony formation assay. Invasion and migration were detected by Transwell assay. The percentage of apoptosis was measured by flow cytometry. The levels of Bax and cleaved Caspase-3 were measured by Western blotting. Results The expression of PHLDA2 was upregulated in HCC, and high expression of PHLDA2 reduced the overall survival of HCC patients. Low-expression of PHLDA2 inhibited proliferation, invasion and migration, and increased apoptosis of HCC cells. Conclusion PHLDA2 promotes the occurrence and development and may act as a tumor promoter in HCC.