p53 suppression is essential for oncogenic SPAG5 upregulation in lung adenocarcinoma.

Aberrant expression of sperm-associated antigen 5 is implicated to play oncogenic roles in several types of cancers. However, the functions of in lung adenocarcinoma remain unclear. In this study, we investigated the role of duanyu1842G5 in lung adenocarcinoma. We found that duanyu1842G5 was upregulated in most of the lung adenocarcinoma cell lines as compared to normal lung epithelial cells. duanyu1842G5 knockdown suppressed proliferation, colony forming, and migration of lung adenocarcinoma A549 cells in vitro and inhibited tumor growth in vivo. These suggest that upregulated duanyu1842G5 promotes lung tumor progression. Importantly, treatment with MDM2 inhibitor, Nutlin-3a, restored p53 and p21 expression and suppressed duanyu1842G5 expression in wild-type p53 lung adenocarcinoma cells, A549 and H460, but not in p53-null lung cancer cells, H1299. This suggests that the p53 signal pathway is essential for duanyu1842G5 suppression. In addition, knocking-down p53 or p21 in A549 and H460 cells attenuated Nutlin-3a-induced repression of which further supports that the p53-p21 axis is required for duanyu1842G5 repression. Thus, duanyu1842G5 can serve as a prognostic marker, and therapeutic strategy targeting the axis may have important clinical implications.

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