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Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform

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The hypofunctional effect of P335L single nucleotide polymorphism on SSTR5 function.

Guisheng Zhou¹, Marie-Claude Gingras, Shi-He Liu

¹Michael E. DeBakey Department of Surgery, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

World Journal of Surgery

|January 21, 2011

Summary

The somatostatin receptor subtype 5 (SSTR5) P335L single nucleotide polymorphism (SNP) is prevalent and race-dependent in pancreatic cancer patients. This SSTR5 P335L variant impairs somatostatin analog efficacy, potentially affecting treatment outcomes.

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Area of Science:

Endocrinology
Oncology
Genetics

Background:

Somatostatin receptor subtype 5 (SSTR5) regulates insulin and cell proliferation.
The SSTR5 P335L single nucleotide polymorphism (SNP) alters the receptor's C-terminal region.
Investigating SSTR5 P335L in pancreatic cancer is crucial for understanding disease mechanisms and treatment response.

Purpose of the Study:

To determine the distribution of the SSTR5 P335L SNP in pancreatic cancer patients across different races.
To assess the functional impact of the SSTR5 P335L SNP on SSTR5 activity in human pancreatic cancer cells.

Main Methods:

Genotyping of 246 pancreatic cancer patients (Caucasians, Hispanics, African Americans) and 17 cell lines using TaqMan SNP assay.
Site-directed mutagenesis to create SSTR5 leucine (L335) and proline (P335) variants.
Cell proliferation (MTS assay) and insulin secretion (ELISA) measurements following transient transfections.

Main Results:

The SSTR5 P335L SNP frequency was race-dependent (Caucasians 52%, Hispanics 69%, African Americans 35%).
Overexpression of SSTR5 L335 enhanced pancreatic cancer cell proliferation and PDX-1 expression.
SSTR5 L335 blocked the inhibitory effects of a somatostatin analog (RPL-1980) on cell proliferation and insulin secretion.

Conclusions:

The SSTR5 P335L SNP is common in the human population and pancreatic cancer patients, with a race-dependent distribution.
The SSTR5 L335 variant exhibits hypofunctional characteristics, promoting proliferation and PDX-1 expression.
This SNP may compromise the efficacy of somatostatin analog therapy in pancreatic cancer patients.