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Somatic mutations in CCK2R alter receptor activity that promote oncogenic phenotypes
Melinda D Willard1, Mary E Lajiness, Isabella H Wulur
1Department of Translational Science, Lilly Research Laboratories, Indianapolis, Indiana 46225, USA. willardme@lilly.com
Molecular Cancer Research : MCR
|April 21, 2012
Summary
Mutations in the cholecystokinin 2 receptor (CCK2R) were found in colorectal and gastric cancers. These CCK2R alterations increase receptor activity, promoting cancer growth and spread.
Area of Science:
- Oncology
- Molecular Biology
- Gastroenterology
Background:
- The cholecystokinin 2 receptor (CCK2R) is involved in gastrointestinal and central nervous system functions.
- Evidence suggests CCK2R alterations may contribute to cancer, but their functional role in tumorigenesis is unclear.
Purpose of the Study:
- To investigate the functional significance of CCK2R alterations in colorectal and gastric cancers.
- To determine if identified CCK2R mutations impact receptor activity and downstream signaling pathways relevant to cancer.
Main Methods:
- Genomic analysis of CCK2R in 140 colorectal and 44 gastric cancer samples.
- Functional assays to assess the impact of CCK2R mutations on receptor activity, signaling pathways, cell migration, and angiogenesis.
Main Results:
- Six distinct mutations in CCK2R were identified in the cancer samples.
- These mutations were shown to increase CCK2R activity.
- Mutant CCK2R activated downstream signaling, enhanced cell migration, and promoted angiogenesis.
Conclusions:
- Somatic mutations in CCK2R can promote tumorigenesis by deregulating receptor activity.
- CCK2R inhibitors should be evaluated for their efficacy against both normal and mutant CCK2R forms in cancer treatment.
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