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Updated: Oct 7, 2025

Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
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Downregulation of CCKBR Expression Inhibits the Proliferation of Gastric Cancer Cells, Revealing a Potential Target

Meng Li1, Jiang Chang1, Honglin Ren1

  • 1Key Laboratory of Zoonosis Research, Ministry of Education/Institute of Zoonosis/College of Veterinary Medicine, Double-First Class Discipline of Human-Animal Medicine, Jilin University, Changchun 130062, China.

Current Cancer Drug Targets
|January 7, 2022
PubMed
Abstract

Insights

Cholecystokinin B receptor (CCKBR) drives gastric cancer growth and metastasis. Targeting CCKBR with immunotoxins like FQ17P shows promise for gastric cancer therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Cholecystokinin B receptor (CCKBR) expression is elevated in various neoplasms.
  • Gastric cancer (GC) is a significant global health concern with limited therapeutic options.

Purpose of the Study:

  • To investigate the role of CCKBR in driving gastric cancer progression.
  • To evaluate CCKBR as a potential therapeutic target for immunotoxin therapy in GC.

Main Methods:

  • Utilized a lentiviral interference system to generate CCKBR-knockdown GC cells.
  • Assessed cell proliferation, migration, invasion, and cell cycle.
  • Investigated in vivo tumor growth using a xenograft model and evaluated immunotoxin FQ17P cytotoxicity.

Main Results:

  • CCKBR downregulation significantly reduced GC cell proliferation, migration, and invasion in vitro.
  • CCKBR knockdown inhibited gastric tumor growth in vivo.
  • Immunotoxin FQ17P demonstrated specific cytotoxicity against CCKBR-overexpressing GC cells.

Conclusions:

  • CCKBR protein promotes gastric cancer growth, migration, and invasion.
  • CCKBR represents a promising therapeutic target for immunotoxin-based strategies in gastric cancer.
Keywords:
CCKBRFQ17Pgastric cancer proliferationimmunotoxinribonucleic acid interferencetargeted therapy

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