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Updated: Oct 26, 2025

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Published on: August 23, 2019
miR-142-5p Inhibits Cell Invasion and Migration by Targeting DNMT1 in Breast Cancer
Hui Li1, Han-Han Li2, Qian Chen3
1Department of Hematology and Nephrology, Tianyou Hospital Affiliated to Wuhan University of Science and TechnologyHubeiP.R. China.
Abstract:
Abnormal cell proliferation caused by abnormal transcription regulation mechanism seems to be one of the reasons for the progression of breast cancer and also the pathological basis. MicroRNA-142-5p (miR-142-5p) is a low-expressed miRNA in breast cancer. The role of MKL-1s regulation of DNMT1 in breast cancer cell proliferation and migration is still unclear. MKL-1 (myocardin related transcription factor A) can bind to the conserved cis-regulatory element CC (A/T) 6GG (called CarG box) in the promoter to regulate the transcription of miR-142-5p. The expressions of miR-142-5p and MKL-1 are positively correlated. In addition, it has been proved that DNMT1 is the target of miR-142-5p, which inhibits the expression of DNMT1 by targeting the 3-UTR of DNMT1, thereby forming a feedback loop and inhibiting the migration and proliferation of breast cancer. Our data provide important and novel insights into the MKL-1/miR-142-5p/DNMT1/maspin signaling pathway and may become a new idea for breast cancer diagnosis, treatment, and prognosis.
Insights
Myocardin related transcription factor A (MKL-1) regulates miR-142-5p, which targets DNMT1. This MKL-1/miR-142-5p/DNMT1 pathway inhibits breast cancer cell proliferation and migration.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Abnormal transcription regulation drives breast cancer progression.
- MicroRNA-142-5p (miR-142-5p) is downregulated in breast cancer.
- The role of MKL-1 in regulating DNMT1 in breast cancer is not well understood.
Purpose of the Study:
- To investigate the regulatory role of MKL-1 on miR-142-5p and its downstream effects on DNMT1 in breast cancer.
- To elucidate the MKL-1/miR-142-5p/DNMT1 signaling pathway in breast cancer cell proliferation and migration.
Main Methods:
- Analysis of MKL-1 binding to the miR-142-5p promoter.
- Correlation analysis of miR-142-5p and MKL-1 expression.
- Validation of DNMT1 as a miR-142-5p target via 3-UTR interaction.
- Assessment of the pathway's impact on breast cancer cell behavior.
Main Results:
- MKL-1 directly regulates miR-142-5p transcription via CarG box binding.
- miR-142-5p and MKL-1 expression levels are positively correlated in breast cancer.
- miR-142-5p inhibits DNMT1 expression by targeting its 3-UTR, forming a feedback loop.
- This pathway significantly inhibits breast cancer cell proliferation and migration.
Conclusions:
- The MKL-1/miR-142-5p/DNMT1 axis plays a crucial role in controlling breast cancer cell growth and metastasis.
- This pathway represents a novel target for breast cancer diagnosis, treatment, and prognosis.
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