New relationship of E2F1 and BNIP3 with caveolin-1 in lung cancer-associated fibroblasts

Thorac Cancer. 2020 Jun;11(6):1369-1371. doi: 10.1111/1759-7714.13408. Epub 2020 Mar 25.

Abstract

In recent years, studies have found that E2F1, a downstream effector of caveolin-1 (Cav-1), participates in tumor cell metabolic reprogramming. E2F1 modulates mitochondrial fusion and mitophagy. Bioinformatic analysis has identified the E2F1-MFN2 axis as a regulator of mitophagy. Our data establish a new novel paradigm for regulation of the tumor cell metabolic reprogramming pathway by Cav-1 that is operationally linked and mutually dependent on the transcriptional activation of E2F1 and induces mitophagy with BNIP3 in cancer-associated fibroblasts (CAFs).

Keywords: BNIP3; E2F1; cancer-associated fibroblasts; caveolin-1; mitophagy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Cancer-Associated Fibroblasts* / metabolism
  • Caveolin 1
  • E2F1 Transcription Factor / metabolism
  • Humans
  • Lung
  • Membrane Proteins / metabolism
  • Mitophagy
  • Neoplasms*
  • Proto-Oncogene Proteins / metabolism

Substances

  • BNIP3 protein, human
  • Caveolin 1
  • E2F1 Transcription Factor
  • E2F1 protein, human
  • Membrane Proteins
  • Proto-Oncogene Proteins