Journal
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
Volume 14, Issue 2, Pages 111-123Publisher
IVYSPRING INT PUBL
DOI: 10.7150/ijbs.23230
Keywords
TGF-beta; SMAD4; tumorigenesis; prognosis; mouse model
Categories
Funding
- University of Macau [CPG2017-00026-FHS, SRG2015-00045-FHS, MYRG2016-00132-FHS, MYRG2016-00139]
- FDCT [065/2015/A2, 094/2015/A3]
- NATIONAL CANCER INSTITUTE [R01CA236591] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [R01AA023146] Funding Source: NIH RePORTER
- Veterans Affairs [I01BX003732] Funding Source: NIH RePORTER
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Transforming growth factor beta (TGF-beta) signaling pathway plays important roles in many biological processes, including cell growth, differentiation, apoptosis, migration, as well as cancer initiation and progression. SMAD4, which serves as the central mediator of TGF-beta signaling, is specifically inactivated in over half of pancreatic duct adenocarcinoma, and varying degrees in many other types of cancers. In the past two decades, multiple studies have revealed that SMAD4 loss on its own does not initiate tumor formation, but can promote tumor progression initiated by other genes, such as KRAS activation in pancreatic duct adenocarcinoma and APC inactivation in colorectal cancer. In other cases, such as skin cancer, loss of SMAD4 plays an important initiating role by disrupting DNA damage response and repair mechanisms and enhance genomic instability, suggesting its distinct roles in different types of tumors. This review lists SMAD4 mutations in various types of cancer and summarizes recent advances on SMAD4 with focuses on the function, signaling pathway, and the possibility of SMAD4 as a prognostic indicator.
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