Tumor Suppressor Inhibits the Progression of Cervical Cancer by Regulating the PTEN/Akt/mTOR Pathway.

OBJECTIVE

Cervical cancer (CC) ranks among the most prevalent malignant tumors affecting the female reproductive system. Nonetheless, various shortcomings exist within current treatment approaches for CC. Therefore, the quest for new intervention targets holds significant importance. Research has demonstrated that long non-coding RNA (lncRNA) long intergenic non-protein coding RNA 2487 () can suppress the development of oral squamous cell carcinoma (OSCC). However, its function and potential mechanisms in CC remain unclear, therefore, this study aims to investigate the role and potential mechanism of in CC.

METHODS

and phosphatase and tensin homolog () expression were assessed using real-time quantitative polymerase chain reaction (RT-qPCR) in CC tissue samples and constructed cell models. was either knocked down or overexpressed, and PTEN was knocked down in the CC (SiHa) cell line via transfection technology. The expression levels of and in SiHa cell lines were examined using RT-qPCR after various treatments. Cell proliferation ability was determined through Cell Counting Kit (CCK)-8 and colony formation assays, while the ability to invade and migrate was assessed via Transwell experiments. Western blot analysis was employed to measure the levels of key proteins in the PTEN/Akt/mechanistic target of the rapamycin (mTOR) signaling pathway.

RESULTS

A positive correlation was observed between and , both of which were found to be downregulated in CC cells and tissues ( < 0.05). experiments demonstrated that overexpression of significantly inhibited colony formation ( < 0.01), invasion ( < 0.01), migration ( < 0.01), and proliferation ( < 0.01) of SiHa cells. Furthermore, overexpression led to upregulation of expression ( < 0.01) and inhibition of the Akt/mTOR signaling pathway ( < 0.01), while knockdown of produced the opposite effect ( < 0.01). Additionally, knocking down counteracted the inhibitory effects of overexpression on CC progression ( < 0.01) and the Akt/mTOR signaling pathway ( < 0.01).

CONCLUSION

findings suggest that may impede the progression of CC by suppressing the Akt/mTOR signaling pathway through the upregulation of expression. Consequently, holds promise as a potential therapeutic target for the treatment of CC.