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Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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Updated: May 17, 2026

Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells
10:04

Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells

Published on: August 1, 2025

Tumor regression by phenethyl isothiocyanate involves DDB2.

Nilotpal Roy1, Indira Elangovan, Dragana Kopanja

  • 1Department of Biochemistry and Molecular Genetics, Cancer Center, University of Illinois at Chicago, Chicago, IL, USA.

Cancer Biology & Therapy
|November 2, 2012
PubMed
Summary
This summary is machine-generated.

Phenethyl isothiocyanate (PEITC) boosts the DNA repair protein DDB2, crucial for its tumor-suppressing effects. DDB2-deficient tumors do not respond to PEITC, highlighting DDB2

Keywords:
DDB2PEITCROSapoptosiscolon cancerdrug resistancesenescence

Related Experiment Videos

Last Updated: May 17, 2026

Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells
10:04

Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells

Published on: August 1, 2025

Area of Science:

  • Molecular Oncology
  • Cancer Chemoprevention
  • DNA Repair Mechanisms

Background:

  • Phenethyl isothiocyanate (PEITC), found in cruciferous vegetables, shows promise as a cancer chemopreventive and therapeutic agent.
  • DDB2 (damaged DNA binding protein 2) is a DNA repair protein involved in apoptosis and senescence, with attenuated expression in various cancers, including colon cancer.
  • The precise mechanism by which PEITC exerts its tumor-suppressive effects requires further elucidation.

Purpose of the Study:

  • To investigate the role of DDB2 in the tumor suppressive effects of PEITC.
  • To determine the molecular pathways involved in PEITC-induced DDB2 expression.
  • To assess the efficacy of PEITC in tumors with varying DDB2 expression levels.

Main Methods:

  • Treatment of colon cancer cells with PEITC.
  • Analysis of DDB2 expression and its regulation via reactive oxygen species and the p38MAPK/JNK pathway.
  • Evaluation of tumor progression in DDB2-deficient versus DDB2-proficient colon cancer models treated with PEITC.

Main Results:

  • PEITC treatment significantly increases DDB2 expression in colon cancer cells.
  • PEITC-induced reactive oxygen species augment DDB2 expression through the p38MAPK/JNK pathway, independent of p53.
  • DDB2-deficient colon cancer tumors are refractory to PEITC, exhibiting deficiencies in apoptosis and senescence, while DDB2-proficient tumors respond effectively.

Conclusions:

  • PEITC's tumor suppressive activity is critically dependent on its ability to induce DDB2 expression.
  • DDB2 induction by PEITC is mediated by reactive oxygen species and the p38MAPK/JNK pathway.
  • DDB2 expression is essential for PEITC's therapeutic efficacy in inhibiting colon cancer progression.