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ALLN hinders HCT116 tumor growth through Bax-dependent apoptosis

Shang-ze Li1, Hui-hui Zhang, Jia-nong Zhang

  • 1College of Life Sciences, Wuhan University, Wuhan, Hubei 430072, China.

Biochemical and Biophysical Research Communications
|July 9, 2013
PubMed

Insights

N-acetyl-leu-leunorleucinal (ALLN) inhibits colon cancer growth and promotes apoptosis. This calpain inhibitor works by initiating the Bax translocation to mitochondria, suggesting its potential as a colon cancer prevention agent.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • High expression of cysteine proteases calpain I and II is linked to tumorigenicity.
  • N-acetyl-leu-leunorleucinal (ALLN) inhibits calpain I and II, suggesting a role in tumor growth and carcinogenesis.

Purpose of the Study:

  • To investigate the anti-colon cancer effects of ALLN.
  • To explore ALLN's role in inducing apoptosis in colon cancer cells.

Main Methods:

  • Utilized HCT116 colon cancer cell lines, including p53 and Bax-deficient variants.
  • Assessed cell viability, tumor growth, and apoptosis via flow cytometry.
  • Examined Bax translocation from cytosol to mitochondria.

Main Results:

  • ALLN treatment decreased colon cancer cell viability and tumor growth in a dose-dependent manner.
  • ALLN induced apoptosis in HCT116 cells, dependent on Bax but not p53.
  • ALLN-induced apoptosis involved Bax translocation to mitochondria.

Conclusions:

  • ALLN inhibits colon tumor formation and growth in vivo and in vitro.
  • The mechanism involves apoptosis via the mitochondrial pathway mediated by Bax translocation.
  • ALLN shows promise as a novel agent for colon cancer prevention.
Keywords:
ALLNAnti-tumorApoptosisBaxCCK-8Cell Counting Kit-8Colon cancerMitochondriaN-acetyl-leu-leunorleucinalPBSPVDFphosphate-buffered salinepolyvinylidene difluoride

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