IMPA2 blocks cervical cancer cell apoptosis and induces paclitaxel resistance through p53-mediated AIFM2 regulation.

Cervical cancer continues to be a concern, and the prognosis of locally advanced cervical cancer remains poor. was previously identified as a potential oncogene and regulator of tumor apoptosis. In this study, we aim to further elucidate the underlying mechanisms of gene in the regulation of cervical cancer apoptosis. First, we identify as an upregulated gene in -silenced cervical cancer cells, and inhibition of reverses knockdown-induced apoptosis. Further study reveals that regulates cell apoptosis in a mitochondrial-dependent manner with a redistribution of mitochondrial membrane potential and intracellular Ca levels. However, the analysis of the STRING database and our experimental results show that has little effect on cervical cancer progression and survival. Further mechanistic study demonstrates that and silencing inhibits apoptosis by activating p53. Meanwhile, the knockdown of enhances the chemosensitivity of cervical cancer cells by strengthening paclitaxel-induced apoptosis. Based on the above results, the IMPA2/AIFM2/p53 pathway may be a new molecular mechanism for paclitaxel treatment of cervical cancer and an effective strategy to enhance the sensitivity of cervical cancer cells to paclitaxel. Our findings display a novel function of in regulating cell apoptosis and paclitaxel resistance mediated by a disturbance of and expression, potentially making it a novel therapeutic target for cervical cancer treatment.