The early metastasis of cervical cancer is a multi-step process requiring the cancer cells to adapt to the signal input from different tissue environments, including hypoxia. Hypoxia-induced epithelial-to-mesenchymal transition (EMT) plays a critical role in the acquisition of the ability to invade surrounding tissue. However, the molecular mechanism underlying EMT in cervical cancer remains to be elucidated. Herein, we showed that HIF‑1α and ARNT are recruited to the hCINAP promoter and initiate hCINAP expression in hypoxia. Ablation of hCINAP decreased the migratory capacity and EMT of cervical cancer cells in hypoxia. Furthermore, hCINAP regulates EMT through Akt/mTOR signaling and inhibits hypoxia-induced p53-dependent apoptosis. Our data collectively showed that hCINAP may have essential roles in the metastasis of cervical cancer and could be a potential target for curing cervical cancer.
Hypoxia and TGF-β1 induced PLOD2 expression improve the migration and invasion of cervical cancer cells by promoting epithelial-to-mesenchymal transition (EMT) and focal adhesion formation
