Research Paper
Exploration of miR-22 inhibiting cervical cancer progression through suppressing TGF-β/Smad3 pathway by targeting TGFBR1
- 1 Department of Obstetrics and Gynecology, Shanghai Pudong New Area People’s Hospital, Shanghai 201200, China
Received: December 11, 2023 Accepted: April 9, 2024
https://doi.org/10.18632/aging.How to Cite
Copyright: © 2024 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background: The TGF-β/Smad3 pathway is frequently active in cervical cancer, preventing tumor cell apoptosis and fostering tumor cell survival and growth. According to reports, miR-22 inhibits the activation of the TGF-β/Smad3 pathway by targeting the TGF-β receptor TGFBR1. The therapeutic potential of miR-22 in cervical cancer has also been reported. However, the relationship between the two has not been fully studied.
Methods: Through clinicopathological tissue examination and in vitro tests, this study will investigate the link between miR-22 and TGF-β/Smad3 pathway expression. Collect cervical cancer tissues and para-cancerous tissues from patients, and compare the expression of miR-22 and TGF-β/Smad3 pathway. Hela cell lines were used as cell models for in vitro experiments. Cell lines overexpressing/inhibiting miR-22 (miR-22 mimic/inhibitor) and TGFBR1 overexpressing (oe-TGFBR1) were cultivated by cell transfection. Cell proliferation was detected by colony formation. Cell migration was discovered using the cell scratch test. Cell apoptosis was discovered using flow cytometry. Dual luciferase reporter assay was used to confirm the binding of miR-22 and TGFBR1. TGFBR1, TGF-β1, and Smad3 mRNA expression levels were identified using RT-PCR. TGFBR1, TGF-β1, and Smad3 protein expression was found using Western blot.
Results: Significantly less miR-22 was expressed in cervical carcinoma tissue. Hela cell growth was suppressed and cell apoptosis was aided by miR-22 overexpression. The TGF-β/Smad3 pathway was blocked by miR-22 overexpression. TGFBR1 was the binding target of miR-22. Overexpression of TGFBR1 reversed the effect of overexpression of miR-22 on Hela cells. Overexpression of TGFBR1 reversed the inhibition of TGF-β/Smad3 pathway by overexpression of miR-22.
Conclusion: In this work, thorough clinical and in vitro cell studies were performed to show that miR-22 suppressed the expression of the TGF-β/Smad3 pathway by targeting TGFBR1, consequently decreasing cervical cancer cell growth and increasing death.