Yeannie Hui‐Yeng YapYee‐How Say2024-12-272024-12-272012-0310.1042/CBI20110088https://dspace-cris.utar.edu.my/handle/123456789/8464Since the discovery of PrP<sup>C</sup> (cellular prion protein), most studies have focused on its role in neurodegenerative diseases, whereas its function outside the nervous system remains obscure. We investigated the ability of PrP<sup>C</sup> in resisting TNFα (tumour necrosis factor α) apoptosis in three PrP<sup>C</sup>‐transiently transfected cancer cell lines, renal adenocarcinoma ACHN, oral squamous cell carcinoma HSC‐2 and colon adenocarcinoma LS174T. PrP<sup>C</sup>‐expressing ACHN and LS174T cells had higher viabilities compared with the mock‐transfected cells, while the transient overexpression of PrP<sup>C</sup> had minimal overall effect on HSC‐2 cells due to its high endogenous PrP<sup>C</sup> expression. Cell cycles were also analysed, with both PrP<sup>C</sup> expressing ACHN and LS174T cells having a significantly higher proliferative index than mock‐transfected cells. Flow cytometry analysis indicated a G<sub>1</sub>/S‐phase cell cycle transition in both PrP<sup>C</sup>‐expressing ACHN and LS174T cells. PrP<sup>C</sup> resists TNFα apoptosis due to a modest, but statistically significant, cell‐specific cytoprotection compared with mock‐transfected cells.Resistance against tumour necrosis factor α apoptosis by the cellular prion protein is cell‐specific for oral, colon and kidney cancer cell linesjournal-article