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MicroRNA-543 suppresses endometrial cancer oncogenicity via targeting FAK and TWIST1 expression

  • Gynecologic Oncology
  • Published:
Archives of Gynecology and Obstetrics Aims and scope Submit manuscript

Abstract

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.

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Abbreviations

FAK:

Focal adhesion kinase

TWIST1:

Twist homolog 1

miRNA:

MicroRNA

BrdU:

5-Bromo-2-deoxyuridine

EMT:

Epithelial mesenchymal transition

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Acknowledgments

This work was supported by the Natural Scientific Research Fund of China (No. 81100916).

Conflict of interest

We declare that we have no conflict of interests.

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Corresponding author

Correspondence to Gao Wei.

Additional information

Dr. C. Hong and Dr. L. Bing contributed equally to this study.

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Bing, L., Hong, C., Li-Xin, S. et al. MicroRNA-543 suppresses endometrial cancer oncogenicity via targeting FAK and TWIST1 expression. Arch Gynecol Obstet 290, 533–541 (2014). https://doi.org/10.1007/s00404-014-3219-3

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  • DOI: https://doi.org/10.1007/s00404-014-3219-3

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