Effect of MiR-10b on Cervical Cancer Rats Through mTOR/P70S6K Signaling Pathway

Area of Science:

• Oncology
• Molecular Biology
• Immunology

Background:

• Cervical cancer (CC) remains a significant global health challenge.
• Understanding the molecular mechanisms underlying CC development is crucial for targeted therapies.

Purpose of the Study:

• To investigate the biological effects and underlying mechanisms of microRNA-10b (miR-10b) in a rat model of cervical cancer.
• To elucidate the role of miR-10b in regulating inflammation, oxidative stress, immune response, and cell apoptosis in CC.

Main Methods:

• Establishment of a rat model of cervical cancer, divided into Inhibitors, Mimics, and Control groups.
• Analysis of miR-10b expression, immune cell markers (CD3+, CD4+, CD8+), inflammatory cytokines (IL-8, TNF-β, IL-6), oxidative stress markers (CAT, SOD, MDA), and apoptosis via RT-PCR, ELISA, and TUNEL assay.
• Assessment of apoptosis-related genes (Caspase-3, Bcl-2) and the mTOR/P70S6K signaling pathway at both mRNA and protein levels using qRT-PCR and Western blotting.

Main Results:

• miR-10b levels were significantly altered in Inhibitors and Mimics groups, correlating with changes in inflammatory markers, oxidative stress, and immune cell content.
• The Mimics group exhibited increased apoptosis and elevated immune factors, while the Inhibitors group showed decreased apoptosis and altered inflammatory/oxidative stress profiles.
• miR-10b modulated the expression of Bcl-2, Caspase-3, and significantly suppressed the mTOR/P70S6K pathway at both mRNA and protein levels.

Conclusions:

• miR-10b plays an inhibitory role in the occurrence and development of cervical cancer in rats.
• The mechanism involves the suppression of the mTOR/P70S6K signaling pathway, reduction of inflammation and oxidative stress, and enhancement of immune factor levels.