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Autophagy and cellular senescence mediated by Sox2 suppress malignancy of cancer cells

Yong-Yeon Cho1, Dong Joon Kim, Hye Suk Lee

  • 1College of Pharmacy, The Catholic University of Korea, Gyeonggi-do, Korea. yongyeon@catholic.ac.kr

Plos One
|March 2, 2013
PubMed

Insights

The transcription factor Sox2 promotes autophagy in colon cancer cells by increasing ATG10 expression. This autophagy inhibits cancer cell proliferation and tumor growth, offering a potential new treatment strategy.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Autophagy is vital for cellular homeostasis but its role in cancer remains unclear.
  • Sox2 is a transcription factor regulating stemness in embryonic and induced-pluripotent stem cells.

Purpose of the Study:

  • To investigate the role of Sox2 in regulating autophagy in colon cancer cells.
  • To determine the molecular mechanisms and therapeutic potential of Sox2-mediated autophagy in colon cancer.

Main Methods:

  • Assessed autophagic phenomena (vacuole formation, lysosomal activation) in colon cancer cells.
  • Analyzed Sox2-mediated ATG10 gene expression.
  • Evaluated the impact of Sox2 and ATG10 on cell proliferation, colony formation, and tumor growth in vivo.
  • Investigated the effect of Sox2-induced autophagy on cellular senescence markers (p16INK4a, p21, p53).

Main Results:

  • Sox2 strongly induced autophagy in colon cancer cells via ATG10.
  • Sox2-induced autophagy inhibited cell proliferation, anchorage-independent growth, and tumor growth.
  • Sox2-mediated autophagy enhanced cellular senescence by upregulating p16INK4a, p21, and p53.
  • Knockdown of ATG10 reversed the anti-cancer effects in Sox2-expressing cells.

Conclusions:

  • Sox2 regulates autophagy in colon cancer through ATG10.
  • Sox2-induced autophagy inhibits colon cancer progression and promotes senescence.
  • Targeting Sox2-mediated autophagy presents a novel therapeutic strategy for human colon cancers.

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