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Updated: Jun 7, 2025

Development of Compendium for Esophageal Squamous Cell Carcinoma
03:36

Development of Compendium for Esophageal Squamous Cell Carcinoma

Published on: April 12, 2024

383

Cellular communication network 1 promotes CASP2 mRNA expression but suppresses its protein translation in esophageal

Ruize Xu1, Zhenyu Jiang1, Xianmei Meng1

  • 1Inner Mongolia Institute of Digestive Diseases Inner Mongolia Engineering Research Center for Prevention and Treatment of Digestive Diseases The Second Affiliated Hospital of Baotou Medical College Inner Mongolia University of Science and Technology Baotou China.

Journal of Cell Communication and Signaling
|November 11, 2024
PubMed

Insights

Cellular communication network 1 (CCN1) induces apoptosis in esophageal adenocarcinoma by promoting caspase-3 (CASP3) activation, not caspase-2 (CASP2), despite increased CASP2 transcription. CCN1 enhances CASP3 expression and activation, crucial for cancer cell death.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • Apoptosis induction is a key cancer treatment strategy.
  • Caspase-2 (CASP2) can initiate apoptosis independently.
  • Cellular communication network 1 (CCN1) has dual roles in cancer, suppressing esophageal adenocarcinoma (EAC).

Purpose of the Study:

  • To investigate the role of CCN1 in inducing apoptosis in EAC cells.
  • To elucidate the mechanisms by which CCN1 affects CASP2 and CASP3 in EAC.

Main Methods:

  • Analysis of CCN1's effect on CASP2 transcription and translation.
  • Investigation of CCN1's impact on p16, p21, RB1 phosphorylation, E2F1, and HuR.
  • Assessment of CCN1's influence on CASP3 transcription, translation, and activation.

Main Results:

  • CCN1 upregulated CASP2 transcription but inhibited its translation in EAC cells via p16/p21/RB1/E2F1 and HuR pathways.
  • CASP2 did not contribute to CCN1-induced apoptosis in EAC.
  • CCN1 promoted CASP3 transcription, translation, and activation, driving EAC cell apoptosis.

Conclusions:

  • CCN1 induces apoptosis in EAC cells primarily through CASP3 activation.
  • The interplay between CCN1, cell cycle regulators, and HuR dictates CASP2's non-involvement in CCN1-mediated apoptosis.
  • Targeting CCN1-mediated CASP3 activation may offer a therapeutic strategy for EAC.
Keywords:
CASP2CASP3CCN1apoptosisesophageal adenocarcinoma

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