Introduction To determine the mechanism affecting cell deaths for tumor suppression gene-PTEN by targeting EZH2 activity as a therapeutic strategy against EGFR inhibitor resistance in the EGFR-Mutant cervical cancer cell line with radiation-treatment resistance

Methods We investigated the mechanism affecting cell deaths for tumor suppression gene-PTEN by targeting EZH2 activity as a therapeutic strategy against EGFR inhibitor resistance in the EGFR-Mutant cervical cancer cell line with radiation-treatment resistance. Epidermal growth factor receptor (EGFR) expression is expressed in various types of tumors, including cervical cancer, in an increased state than normal tissue.

Results EGFR was expressed in the human cervical cancer cell line (Hela cell line) and cervical cancer radiation-resistant cell line (Hela-R cell line), and it was observed that the Hela cell line disappeared by drug-reacting EGFR inhibitor (Apatinib), but the Hela-R cell line did not die. Therefore, it can be inferred that HelLa-R cell lines generally have pathways other than EGFR-related signaling cascades (e.g., PI3K/Akt, STAT, and MAPK), which have become interesting in EGFR/PI3K/PTEN/AKT signaling pathways, which serve as PETN tumor suppressors. The role of the PTEN gene in the carcinogenesis of cervical cancer is not well known. PIP3 generated by activation of PI3K is converted from PIP3 to PIP2 again by PTEN and SHIP, thus inhibiting the signaling pathway activated by PIP3.

Conclusion/Implications In this study, PTEN and EZH2 can be observed in cervical cancer tissues with radiation resistance. Therefore, the Inhibitor of EZH2 ultimately provides clues about the new chemotherapy’s role in palliative cervical cancer patients with radiation resistance.