Downregulation of gasdermin D promotes gastric cancer proliferation by regulating cell cycle‐related proteins

Downregulation of gasdermin D promotes gastric cancer proliferation by regulating cell... INTRODUCTIONGastric cancer (GC) is the fourth most common cancer in man and the fifth most common cancer in women worldwide, with a high mortality. It is a multifactorial disorder that results from abnormal activation of several oncogenic signaling pathways, the activation of oncogenes, the inactivation of tumor suppressor genes and the dysregulation of cell cycle‐related proteins. However, the molecular mechanism underlying GC remains unclear.Programmed cell death, a genetically controlled process that regulates the regeneration and differentiation of gastric epithelial cells, is important for understanding the carcinogenesis of GC. As a newly found programmed cell death agent, pyroptosis is involved in various diseases, but few studies have been published regarding the relationship between pyroptosis and GC. Recent studies have focused on the gasdermin D (GSDMD) protein, which acts as the trigger of pyroptosis to maintain cell homeostasis. The collapse of this suicide process in the gastric epithelium is considered the cause of GC cell proliferation.Previous studies have shown that in upper gastrointestinal (GI) cancers the expression and function of four gasdermin (GSDM) family genes differed from each other. The GSDM family has been found to participate in the apoptotic signaling to suppress the development of GC. Furthermore, inflammasomes, functioning in http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Digestive Diseases Wiley

Downregulation of gasdermin D promotes gastric cancer proliferation by regulating cell cycle‐related proteins

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Publisher
Wiley Subscription Services, Inc., A Wiley Company
Copyright
© 2018 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd
ISSN
1751-2972
eISSN
1751-2980
D.O.I.
10.1111/1751-2980.12576
Publisher site
See Article on Publisher Site

Abstract

INTRODUCTIONGastric cancer (GC) is the fourth most common cancer in man and the fifth most common cancer in women worldwide, with a high mortality. It is a multifactorial disorder that results from abnormal activation of several oncogenic signaling pathways, the activation of oncogenes, the inactivation of tumor suppressor genes and the dysregulation of cell cycle‐related proteins. However, the molecular mechanism underlying GC remains unclear.Programmed cell death, a genetically controlled process that regulates the regeneration and differentiation of gastric epithelial cells, is important for understanding the carcinogenesis of GC. As a newly found programmed cell death agent, pyroptosis is involved in various diseases, but few studies have been published regarding the relationship between pyroptosis and GC. Recent studies have focused on the gasdermin D (GSDMD) protein, which acts as the trigger of pyroptosis to maintain cell homeostasis. The collapse of this suicide process in the gastric epithelium is considered the cause of GC cell proliferation.Previous studies have shown that in upper gastrointestinal (GI) cancers the expression and function of four gasdermin (GSDM) family genes differed from each other. The GSDM family has been found to participate in the apoptotic signaling to suppress the development of GC. Furthermore, inflammasomes, functioning in

Journal

Journal of Digestive DiseasesWiley

Published: Jan 1, 2018

Keywords: ; ; ; ; ;

References

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