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eIF4E‑related miR‑320a and miR‑340‑5p inhibit endometrial carcinoma cell metastatic capability by preventing

Han-Han Zhang1, Ran Li2, You-Jie Li3

  • 1Core Laboratory Glycobiol and Glycoengn, College of Basic Medical Sciences, Dalian Medical University, Dalian, Liaoning 116044, P.R. China.

Oncology Reports
|January 3, 2020
PubMed

Insights

MicroRNAs miR-320a and miR-340-5p suppress endometrial cancer (EC) metastasis by downregulating the oncogene eukaryotic translation initiation factor 4E (eIF4E). These microRNAs inhibit cell migration and invasion, offering potential therapeutic targets for EC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • Endometrial cancer (EC) metastasis is a primary cause of treatment failure.
  • Eukaryotic translation initiation factor 4E (eIF4E), an oncogene, is overexpressed in various cancers, including EC, correlating with poor prognosis.
  • MicroRNAs (miRNAs) are implicated in cancer development, with some acting as tumor suppressors.

Purpose of the Study:

  • To investigate the role of eIF4E, miR-320a, and miR-340-5p in endometrial cancer.
  • To determine the relationship between eIF4E expression and EC prognosis and grade.
  • To elucidate the mechanism by which miR-320a and miR-340-5p affect EC cell behavior and metastasis.

Main Methods:

  • Analysis of microarray data from the Oncomine database for eIF4E expression in EC.
  • Quantitative analysis of miR-320a and miR-340-5p expression in EC tissues.
  • In vitro studies involving miRNA transfection in EC cells (HEC-1A) to assess effects on migration, invasion, and gene expression.
  • Western blot analysis to detect eIF4E and phosphorylated eIF4E (p-eIF4E) levels.
  • Assessment of matrix metallopeptidase (MMP)-3 and MMP-9 expression.
  • Investigation of the interaction with transforming growth factor β1 (TGF-β1) signaling and epithelial-mesenchymal transition (EMT).

Main Results:

  • High eIF4E expression was associated with poor prognosis and higher pathological grade in EC.
  • eIF4E expression was significantly upregulated in EC tissues compared to normal tissues.
  • miR-320a and miR-340-5p were downregulated in EC tissues.
  • Overexpression of miR-320a or miR-340-5p reduced EC cell migration and invasion by downregulating eIF4E, p-eIF4E, MMP-3, and MMP-9.
  • These miRNAs inhibited TGF-β1-induced EMT and p-eIF4E phosphorylation.

Conclusions:

  • eIF4E is upregulated in EC and linked to adverse outcomes.
  • miR-320a and miR-340-5p act as tumor suppressors in EC by targeting eIF4E.
  • These miRNAs inhibit EC cell metastasis and EMT, suggesting their potential as therapeutic agents.
Keywords:
microRNAendometrial cancereukaryotic translationinitiation factor 4Ecell metastasisepithelial-mesenchymal transitiontransforming growth factor β1

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