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Epithelial to Mesenchymal Transition and Cell Biology of Molecular Regulation in Endometrial Carcinogenesis

Hsiao-Chen Chiu1,2, Chia-Jung Li3, Giou-Teng Yiang4,5

  • 1Department of Obstetrics and Gynecology, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taipei 231, Taiwan. 97311141@gms.tcu.edu.tw.

Journal of Clinical Medicine
|April 3, 2019
PubMed

Insights

Endometrial carcinogenesis involves key signaling pathways like PI3K/AKT and WNT/β-catenin, driving tumor growth and metastasis. Understanding these molecular mechanisms, particularly epithelial-to-mesenchymal transition (EMT), offers new therapeutic targets for endometrial cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Endometrial carcinogenesis is a complex, multi-step process driven by aberrant signaling pathways.
  • Key pathways implicated include PI3K/AKT, Ras/Raf/MEK/ERK, WNT/β-catenin, and vascular endothelial growth factor (VEGF).
  • Genetic and mitochondrial DNA mutations contribute to uncontrolled cell proliferation, apoptosis resistance, and metastasis.

Purpose of the Study:

  • To review current research on the molecular regulation of endometrial carcinogenesis.
  • To specifically focus on the role of epithelial-to-mesenchymal transition (EMT) in endometrial cancer progression.
  • To identify potential novel therapeutic targets for anti-carcinogenesis treatments.

Main Methods:

  • Literature review of clinical and basic research.
  • Analysis of molecular signaling pathways involved in endometrial cancer.
  • Examination of the role of genetic mutations and hormonal signaling in carcinogenesis.

Main Results:

  • The PI3K/AKT pathway, along with TGF-β, promotes endothelial-to-mesenchymal transition (EMT).
  • EMT-associated factors are upregulated through interactions within these signaling cascades.
  • Estrogen and progesterone signaling significantly influence EMT and endometrial cancer prognosis.

Conclusions:

  • Detailed understanding of molecular mechanisms, especially EMT, is crucial for endometrial cancer treatment.
  • Targeting specific signaling pathways and EMT processes may offer novel therapeutic strategies.
  • Further research into these molecular targets holds promise for improving anti-carcinogenesis therapies.
Keywords:
AKT/PI3KRas/Raf/MEK/ERKWNT/β-cateninendometrial cancerepithelial-mesenchymal transition

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