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Epigenetic suppression of FBXL7 promotes metastasis

Loredana Moro1,2,3, Michele Pagano1,2,4

  • 1Department of Biochemistry and Molecular Pharmacology, New York University Grossman School of Medicine, New York, NY, USA.

Molecular & Cellular Oncology
|November 25, 2020
PubMed

Insights

Epigenetic silencing of the FBXL7 gene promotes cancer metastasis. This occurs through promoter methylation, leading to increased active c-SRC, driving epithelial-to-mesenchymal transition and cancer cell invasion.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Epigenetic reprogramming is increasingly recognized as a critical factor in cancer metastasis.
  • Understanding the molecular mechanisms driving metastasis is crucial for developing targeted therapies.

Purpose of the Study:

  • To identify novel epigenetic regulatory mechanisms involved in cancer metastasis.
  • To elucidate the role of F-box/LRR-repeat protein 7 (FBXL7) in metastasis.

Main Methods:

  • Analysis of gene promoter methylation patterns.
  • Assessment of epigenetic silencing of the FBXL7 gene.
  • Investigation of the downstream effects of FBXL7 silencing on c-SRC activity.
  • Evaluation of epithelial-to-mesenchymal transition (EMT) markers and cancer cell invasion assays.

Main Results:

  • Promoter methylation led to epigenetic silencing of the FBXL7 gene.
  • Silencing of FBXL7 resulted in the accumulation of active c-SRC.
  • Activated c-SRC promoted epithelial-to-mesenchymal transition.
  • These molecular events enhanced cancer cell invasion and metastasis.

Conclusions:

  • A novel mechanism linking promoter methylation, FBXL7 silencing, and c-SRC activation in metastasis was identified.
  • This pathway represents a potential therapeutic target for inhibiting cancer spread.
  • Epigenetic silencing of FBXL7 is a key driver of cancer cell invasion and metastasis.
Keywords:
Epigeneticsc-SRCepithelial-to-mesenchymal transitionmetastasisubiquitin ligase

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