High-expressed CKS2 is associated with hepatocellular carcinoma cell proliferation through down-regulating PTEN.

BACKGROUND:Hepatocellular carcinoma (HCC) is a product of cumulative genetic, epigenetic, somatic, and endocrine aberrations. Identifying the differentially expressed genes (DEGs) in HCC is of critical importance for diagnosis and treatment. The purpose of the present study was to screen the key genes associated with hepatocellular carcinoma and to investigate the functions underlying hepatocellular carcinoma progression. MATERIALS AND METHODS:The gene expression profile of GSE64041, GSE40367 and GSE60502, including 100 specimens from HCC patients and 92 specimens from normal liver controls, was downloaded from the GEO database. DEGs were screened using the online analysis tool from the GCBI website and validated by Q-PCR and Kaplan-Meier survival analysis. After knockdown by siRNA in HepG2/C3A and Bel7402 HCC cells, the CCK-8 assay and colony formation assay were used to measure the clonogenic capacity of the tumor cells. Western blotting assay was used to measure the expression of PTEN. RESULTS:Five up-regulated genes were identified as overlapping genes associated with tumor cell activation. Upon validation by Q-PCR and Kaplan-Meier survival analysis, CKS2 was selected for further study. Although the results of CCK-8 did not show a significant difference, the colony formation assay results indicated that the silencing of CKS2 significantly inhibited cancer cell proliferation. Further study found that CKS2 knockdown induced PTEN up-regulation and may associate with P53 pathway activation. CONCLUSION:These findings indicated that CKS2 play a role in tumor activation and serve as a useful potential target for the treatment of HCC.

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