Cip2a induces arginine biosynthesis and promotes tumor progression in non-small cell lung cancer

Cancerous inhibitor of protein phosphatase 2A (Cip2a) is an oncoprotein, playing important roles in tumor progression. However, the underlying mechanisms by which Cip2a promotes tumor aggressiveness in NSCLC remain to be further investigated. In this study, we found that Cip2a expression is elevated in NSCLC and correlates with poor prognosis. Knockdown of Cip2a significantly reduced the ability of cell proliferation, invasion, and metastasis of NSCLC both in vitro and in vivo. Furthermore, we found that Cip2a promotes tumor progression partly by inducing arginine biosynthesis, and knockdown of Cip2a exhibited a significantly increased sensitivity to arginine deprivation and mTOR inhibition. In addition, we found that p53 mutants in NSCLC cells increased Cip2a expression by inhibiting the activity of wild-type p53. Our findings provide new insights into the mechanisms of Cip2a in promoting tumor progression and suggest that Cip2a represents a potential therapeutic target for treating NSCLC.

Automated summary

Cancerous inhibitor of protein phosphatase 2A (Cip2a) is an oncoprotein that plays a crucial role in promoting tumor aggressiveness in non-small cell lung cancer (NSCLC). The study found that elevated Cip2a expression in NSCLC is associated with poor prognosis. Knockdown of Cip2a significantly inhibited cell proliferation, invasion, and metastasis of NSCLC both in vitro and in vivo. Furthermore, it was discovered that Cip2a promotes tumor progression by inducing arginine biosynthesis and its knockdown increases sensitivity to arginine deprivation and mTOR inhibition. In addition, p53 mutants in NSCLC cells increase Cip2a expression by inhibiting wild-type p53 activity. The findings provide valuable insights into the mechanisms of Cip2a in NSCLC and suggest it as a potential therapeutic target.