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DBD-F induces apoptosis in gastric cancer-derived cells through suppressing HIF2α expression

Guang-Hui Tong1, Wei-Wei Tong1, Xiao-Song Qin1

  • 1Department of Laboratory Medicine, ShengJing Affiliated Hospital, China Medical University, Shenyang, 110004, China.

Cellular Oncology (Dordrecht, Netherlands)
|November 4, 2015
PubMed
Abstract

Insights

The novel compound DBD-F demonstrates significant anti-cancer properties against human gastric cancer cells. It effectively induces apoptosis and inhibits tumor growth by targeting HIF2α expression through the MEK/ERK pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Gastric cancer is a leading cause of cancer death in China.
  • Hypoxia-inducible factor 2 alpha (HIF2α) is implicated in gastric cancer aggressiveness.
  • Benzoxadiazole antagonists can interact with HIF2α.

Purpose of the Study:

  • To investigate the anti-tumor effects of 4-(N,Ndimethylaminosulphonyl)-7-fluoro-1,2,3-benzoxadiazole (DBD-F) on human gastric cancer cells.
  • To explore the mechanism of action of DBD-F, including its effect on HIF2α expression and related signaling pathways.

Main Methods:

  • In vitro assays using human gastric cancer cell lines (MKN28 and MKN45).
  • In vivo studies using gastric cancer-derived xenograft models.
  • Analysis of apoptosis, cell mobility, tumor growth, and HIF2α expression.

Main Results:

  • DBD-F induced apoptosis and inhibited mobility in gastric cancer cells in vitro.
  • DBD-F suppressed tumor growth in vivo xenograft models.
  • DBD-F inhibited HIF2α expression in gastric cancer cells.

Conclusions:

  • DBD-F exhibits cytotoxicity and induces apoptosis in gastric cancer cells.
  • DBD-F's mechanism involves the MEK/ERK signaling pathway.
  • DBD-F inhibits HIF2α expression by modulating MEK/ERK phosphorylation.
Keywords:
ApoptosisDBD-FGastric cancerHIF2αMEK/ERK

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