As reported before, aberrant expression of proteins associated with signaling pathways, such as phosphatidylinositol 3-kinase(PI3K), EGF-R, β-catenin, and Erk and Bcl-2 was discovered in CC.
Taken together, these findings indicated that OST could be used as a potential sensitizer to reverse chemoresistance of cisplatin-resistant cervical cancer to cisplatin through repressing NRF2 expression partly associated with PI3K/AKT blockage.
Our study suggests that R7 is a promising chemotherapeutic agent for the treatment of cervical cancer and other PI3K/PTEN/Akt/mTOR signaling-associated tumors.
Current research elucidated that MFI2 promoted cell proliferation, cell metastasis and inhibited cell apoptosis in cervical cancer by regulating the PI3K/AKT signaling pathway.
Seventy percent of patients with endometrial cancer and more than 50% of patients with breast, prostate, anal, hepatocellular, colorectal, and cervical cancer exhibited alterations in at least 1 PI3K pathway gene and/or gene product.
The combined use of BMN673 and BYL719 may serve as a promising therapeutic strategy for patients with cervical cancer exhibiting aberrant PI3K activation.
We suggest that SKA3 overexpression contributes to CC cell growth and migration by promoting cell cycle progression and activating the PI3K-Akt signaling pathway, which may provide potential novel therapeutic targets for CC treatment.
The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) protein is principally involved in the homeostatic maintenance of PI3K/Akt signaling and PTEN has been identified to play an important role in the occurrence and development of cervical cancer.