ESM1 suppresses LncRNA GAS5/miR-23a-3p/PTEN axis to promote the cisplatin-chemotherapy resistance of ovarian cancer cells via activating the PI3K/AKT pathway.

ABSTRACT:

Background

Cisplatin chemotherapy is an important treatment for advanced ovarian cancer (OC). However, the development of cisplatin resistance greatly limits the survival time of OC patients. Endothelial cell-specific molecule 1 (ESM1) has been found to be an important proto-oncogene promoting OC, but its mediating OC cisplatin resistance remains unknown.

Methods

We used quantitative polymerase chain reaction (qPCR) to measure transcription levels of ESM1, Growth arrest specific transcript 5 (GAS5), miR-23a-3p, and Phosphatase And Tensin Homolog (PTEN). A double luciferase reporter gene assay confirmed the direct binding of GAS5 to miR-23a-3p and miR-23a-3p to PTEN mRNA. The effects of ESM1, GAS5, miR-23a-3p, and PTEN on OC cisplatin resistance were tested with an Half Maxim

SUBMITTER: Li H 

PROVIDER: S-EPMC11911279 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature