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Updated: Jul 18, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
microRNA-92b-3p augments colon cancer development through inhibiting KLF3
1Department of Gastrointestinal Surgery, Liaocheng People's Hospital, Liaocheng, Shandong, China.
Abstract:
Colon cancer (CC) is a tumor of the large intestine. miR-92b-3p is often deregulated in the tumorigensis. Here, the role of miR-92b-3p in the development of CC was investigated. miR-92b-3p and Kruppel-like factor 3 (KLF3) expression was examined in CC tissues and cells. miR-92b-3p inhibitor or KLF3 overexpression vector was transfected into CC cells, respectively to observe its role in CC cell proliferation, invasion, migration, and apoptosis. The targeting relationship between miR-92b-3p and KLF3 was validated. Meanwhile, rescue experiments were performed by co-transfection of miR-92b-3p inhibitor and KLF3 siRNA, followed by determining CC cell proliferation, invasion, migration, and apoptosis. Higher miR-92b-3p and lower KLF3 expression levels were observed in CC tissues and cells. miR-92b-3p inhibition or KLF3 overexpression reduced proliferation, invasion, and migration whereas induced apoptosis of CC cells. KLF3 was validated to be the target gene of miR-92b-3p. Depletion of KLF3 could reverse the antitumor role of miR-92b-3p inhibition in CC cells. miR-92b-3p augments CC development through inhibiting KLF3, which may confers a novel way to develop future treatment target.
Insights
MicroRNA-92b-3p (miR-92b-3p) promotes colon cancer (CC) development by inhibiting Kruppel-like factor 3 (KLF3). Targeting miR-92b-3p offers a potential therapeutic strategy for CC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Colon cancer (CC) is a significant health concern, with aberrant microRNA expression implicated in its tumorigenesis.
- MicroRNA-92b-3p (miR-92b-3p) has been observed to be frequently deregulated in various cancers, including colon cancer.
Purpose of the Study:
- To investigate the specific role of miR-92b-3p in the development and progression of colon cancer.
- To elucidate the molecular mechanism underlying miR-92b-3p's function in colon cancer, focusing on its interaction with Kruppel-like factor 3 (KLF3).
Main Methods:
- Quantitative real-time PCR (qRT-PCR) was used to assess miR-92b-3p and KLF3 expression levels in colon cancer tissues and cell lines.
- In vitro experiments involved transfecting colon cancer cells with miR-92b-3p inhibitors or KLF3 overexpression vectors to evaluate effects on cell proliferation, invasion, migration, and apoptosis.
- Dual-luciferase reporter assays and Western blotting were employed to validate the targeting relationship between miR-92b-3p and KLF3.
- Rescue experiments were conducted using co-transfection of miR-92b-3p inhibitors and KLF3 siRNA to confirm the functional interaction.
Main Results:
- Colon cancer tissues and cells exhibited significantly higher expression of miR-92b-3p and lower expression of KLF3 compared to normal controls.
- Inhibition of miR-92b-3p or overexpression of KLF3 significantly suppressed colon cancer cell proliferation, invasion, and migration while promoting apoptosis.
- KLF3 was confirmed as a direct target gene of miR-92b-3p.
- The observed anti-tumor effects of miR-92b-3p inhibition were reversed upon KLF3 depletion, highlighting KLF3's critical role in mediating miR-92b-3p's function.
Conclusions:
- miR-92b-3p promotes colon cancer progression by downregulating the expression of its target gene, KLF3.
- The miR-92b-3p/KLF3 axis represents a potential therapeutic target for the treatment of colon cancer.
- Understanding this molecular pathway provides a novel avenue for developing targeted therapies against colon cancer.
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