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Updated: May 1, 2026

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
Published on: April 6, 2012
MicroRNA-543 suppresses endometrial cancer oncogenicity via targeting FAK and TWIST1 expression
Li Bing1, Chen Hong, Shang Li-Xin
1Department of Gynecology and Obstetrics, The Military General Hospital of Beijing PLA, Beijing, 100700, China.
Introduction:
Focal adhesion kinase (FAK) is a critical mediator of extracellular matrix signaling, cell survival, proliferation and motility. Twist homolog 1 (TWIST1) is a transcription factor and serves as a powerful oncogene. Increased FAK and TWIST1 expression are observed in a variety of solid human tumors and correlate with metastasis and poor survival.
Materials And Methods:
Here, we identify miR-543 as a direct regulator of FAK and TWIST1 expression in endometrial cancer.
Results:
Forced expression of miR-543 in endometrial cancer cell lines decreases both endogenous FAK and TWIST1 mRNA and protein levels. Forced expression of miR-543 in aggressive endometrial cancer cell lines also impairs tumor cell monolayer proliferation, anchorage-independent growth, migration and invasion. Endogenous miR-543 expression is decreased in malignant versus normal endometrium tissue and the levels of miR-543 inversely correlate with mRNA levels of FAK and TWIST1.
Conclusions:
miR-543 expression is decreased in endometrial cancer and serves as a tumor suppressor by targeting FAK and TWIST1 expression.
Insights
MicroRNA-543 (miR-543) acts as a tumor suppressor in endometrial cancer by targeting focal adhesion kinase (FAK) and Twist homolog 1 (TWIST1). Lower miR-543 levels correlate with increased FAK and TWIST1, promoting cancer progression.
Area of Science:
- Molecular oncology
- Cancer biology
- Gene regulation
Background:
- Focal adhesion kinase (FAK) and Twist homolog 1 (TWIST1) are oncogenes implicated in tumor progression, metastasis, and poor survival.
- Elevated FAK and TWIST1 expression are observed in various solid human tumors.
Purpose of the Study:
- To investigate the role of miR-543 as a regulator of FAK and TWIST1 in endometrial cancer.
- To determine the functional impact of miR-543 on endometrial cancer cell behavior.
Main Methods:
- Utilized endometrial cancer cell lines for functional studies.
- Assessed the effects of forced miR-543 expression on FAK and TWIST1 mRNA and protein levels.
- Evaluated the impact of miR-543 on cancer cell proliferation, anchorage-independent growth, migration, and invasion.
- Compared miR-543 expression in malignant versus normal endometrial tissues.
Main Results:
- Forced miR-543 expression reduced endogenous FAK and TWIST1 levels in endometrial cancer cells.
- Overexpression of miR-543 inhibited endometrial cancer cell proliferation, anchorage-independent growth, migration, and invasion.
- Endogenous miR-543 levels were decreased in malignant endometrial tissues compared to normal tissues.
- miR-543 levels inversely correlated with FAK and TWIST1 mRNA levels in endometrial cancer.
Conclusions:
- miR-543 functions as a tumor suppressor in endometrial cancer.
- miR-543 targets FAK and TWIST1, thereby inhibiting endometrial cancer progression.
- Decreased miR-543 expression is a characteristic of endometrial cancer and is associated with increased FAK and TWIST1.
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