Abstract
Shp1 is a cytosolic tyrosine phosphatase that regulates a broad range of cellular functions and targets, modulating the flow of information from the cell membrane to the nucleus. While initially studied in the hematopoietic system, research conducted over the past years has expanded our understanding of the biological role of Shp1 to other tissues, proposing it as a novel tumor suppressor gene functionally involved in different hallmarks of cancer. The main mechanism by which Shp1 curbs cancer development and progression is the ability to attenuate and/or terminate signaling pathways controlling cell proliferation, survival, migration, and invasion. Thus, alterations in Shp1 function or expression can contribute to several human diseases, particularly cancer. In cancer cells, Shp1 activity can indeed be affected by mutations or epigenetic silencing that cause failure of Shp1-mediated homeostatic maintenance. This review will discuss the current knowledge of the cellular functions controlled by Shp1 in non-hematopoietic tissues and solid tumors, the mechanisms that regulate Shp1 expression, the role of its mutation/expression status in cancer and its value as potential target for cancer treatment. In addition, we report information gathered from the public available data from The Cancer Genome Atlas (TCGA) database on Shp1 genomic alterations and correlation with survival in solid cancers patients.
Highlights
Colon adenocarcinomaPTPN6 is generally considered as a tumor suppressor gene, Shp could have different roles in tumorigenesis depending on the different biological background
Specialty section: This article was submitted to Molecular and Cellular Oncology, a section of the journal Frontiers in Oncology
Shp1 activity can be affected by mutations or epigenetic silencing that cause failure of Shp1-mediated homeostatic maintenance
Summary
PTPN6 is generally considered as a tumor suppressor gene, Shp could have different roles in tumorigenesis depending on the different biological background This could explain the opposite correlations between Shp expression and overall survival observed in different type of cancers. Shp decreased expression and PTPN6 hypermethylation are associated with tumor staging, pathological differentiation and poor survival in patients with esophageal squamous cell carcinoma [65]. In prostate cancer and high-grade glioma, PTPN6 promoter methylation and reduced expression of Shp correlate with increased malignancy and poor prognosis [72,73,74,75]. These data suggest that PTPN6 methylation in plasma, in combination with clinical analysis, may be a promising biomarker for NSCLC diagnosis and prognosis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
