ADORA2A promotes proliferation and inhibits apoptosis through PI3K/AKT pathway activation in colorectal carcinoma

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Abstract Background：The third most often diagnosed disease globally and the second most prevalent cause of cancer-related death is colorectal cancer (CRC). Numerous human malignancies have been identified to overexpress ADORA2A. However, it is still ambiguous about its function in CRC. Methods: RNA-seq with stable transfected SETDB1 knockdown cells was used to identify the differentially expressed genes. Further, knockdown of ADORA2A in CRC cell lines SW620 and HCT116 were performed with siRNA and overexpression of ADORA2A in SW480 cells were conducted with plasmid. CCK8, colony formation, wound healing and transwell assay were used to detect the effects of cell proliferation, migration and invasion after knockdown and overexpression of ADORA2A. Also, apoptosis was analyzed by flow cytometry, apoptosis-related proteins and key PI3K/AKT pathway proteins were detected using western blotting. Results: ADORA2A was obtained with RNA-seq and played an important role in CRC prognosis. ADORA2A was relatively high expressed in SW620 and HCT116 cell lines compared to SW480 cell line. Knockdown of ADORA2A in SW620 and HCT116 cell lines inhibited cell proliferation, migration and invasion while overexpression of ADORA2A had the opposite results. In addition, ADORA2A also impacted the expression of apoptosis-related proteins, including as Bcl-2, Bax, caspase3 and caspase9, and reduced apoptosis. Furthermore, this process may include the PI3K/AKT signal pathway. Conclusion: ADORA2A promotes CRC progression by PI3K/AKT signaling pathway. It might contribute to management and treatment of CRC.

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