ESCO2 promotes the proliferation of hepatocellular carcinoma through PI3K/AKT/ mTOR signaling pathway

Abstract

Abstract Background: Establishment of sister chromatid cohesion N-Acetyltransferase 2(ESCO2), a gene reported to involved in the establishment of sister chromatid cohesion (SCC) and cell proliferation. We aim to explore how ESCO2 affects the proliferation of hepatocellular carcinoma (HCC). Methods: ESCO2’s expression value and its relationship with clinical prognosis were explored based on TCGA, HCCDB and ICGC databases. We then utilized bioinformatics method analysis to investigate the potential regulatory pathways in which ESCO2 may be implicated. CCK-8, clone assay, and flow cytometry were utilized to examine the impact of ESCO2 knockdown on the malignant biological activity of HCC cells. Finally, we identified the specific regulatory mechanism of ESCO2 using Western blotting. Results: We determined ESCO2 was significantly upregulated in HCC tissues and high ESCO2 expression was linked to a worse prognosis. Bioinformatic analysis revealed that ESCO2 regulated pathways related to the cell cycle and cell proliferation. Furthermore, knockdown of ESCO2 significantly inhibited HCC cell proliferation in vivo and in vitro. Most significantly, ESCO2 stimulates PI3K/AKT/mTOR pathway, which ultimately accelerates up the cell cycle and inhibits apoptosis, promoting the progression of HCC. Conclusion: We revealed the mechanism by which ESCO2 regulates HCC proliferation: ESCO2 promotes HCC proliferation by accelerating the cell cycle and inhibiting apoptosis via the PI3K/AKT/mTOR signaling pathway.