Ell3 functions as a critical decision maker at the crossroad between stem cell senescence and apoptosis

Jae-Yong Lee1, Soo-Hong Lee1, Kwang-Soo Kim1

  • 1Department of Biomedical Science, College of Life Science and CHA Stem Cell Institute, CHA University, 335, Pangyo-ro, Bundang-gu, Seongnam-si, Gyeonggi-do, 463-400, Korea.

Abstract

Insights

Ell3 (elongation factor) regulates stem cell senescence and apoptosis. Its suppression induces senescence via Bcl-2, while overexpression triggers apoptosis, both linked to the p53-Bcl2 axis.

Area of Science:

  • Molecular Biology
  • Stem Cell Biology
  • Cellular Senescence

Background:

  • Ell3 is an RNA polymerase II elongation factor with known roles in stem cell differentiation and cancer therapy.
  • Limited research exists on Ell3's involvement in stem cell senescence and apoptosis.

Purpose of the Study:

  • To investigate the role of Ell3 in regulating stem cell senescence and apoptosis.
  • To elucidate the molecular mechanisms underlying Ell3's function in these processes.

Main Methods:

  • Analysis of stem cell senescence markers (mitochondrial activity, β-gal staining, differentiation efficiency) upon Ell3 suppression.
  • Assessment of stem cell apoptosis using Annexin V staining, immunoblotting, and Live&dead assays for Ell3 overexpression.
  • Chromatin immunoprecipitation and luciferase assays to determine the transcriptional regulation of Ell3 by p53.

Main Results:

  • Ell3 suppression induced stem cell senescence, correlated with increased Bcl-2 expression.
  • Ectopic expression of Ell3 promoted stem cell apoptosis and induced apoptosis in adjacent cells.
  • p53 was identified as a direct transcriptional activator of Ell3.

Conclusions:

  • Ell3 plays a critical role in regulating stem cell senescence and apoptosis.
  • The function of Ell3 in senescent and apoptotic adipose-derived stem cells (ADSCs) is linked to the p53-Bcl2 signaling axis.

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