| General information | Literature | Expression | Regulation | Mutation | Interaction |
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Basic Information |
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|---|---|
Gene ID | 5781 |
Name | PTPN11 |
Synonymous | BPTP3|CFC|NS1|PTP-1D|PTP2C|SH-PTP2|SH-PTP3|SHP2;protein tyrosine phosphatase, non-receptor type 11;PTPN11;protein tyrosine phosphatase, non-receptor type 11 |
Definition | PTP-2C|protein-tyrosine phosphatase 1D|protein-tyrosine phosphatase 2C|tyrosine-protein phosphatase non-receptor type 11 |
Position | 12q24 |
Gene type | protein-coding |
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Title |
Abstract |
| Recovery of anoikis in Src-transformed cells and human breast carcinoma cells by restoration of the SIRP alpha1/SHP-2 signaling system. | Src kinase dysregulation contributes to cancer progression but mechanistic understanding for this contribution remains incomplete. Signal regulatory protein alpha1 (SIRPalpha1) is a tumor suppressor that is constitutively suppressed in v-Src-transformed cells, where restoration of SIRPalpha1 expression inhibits anchorage-independent growth. In this study, we investigated the role of the protein tyrosine phosphatase-2 (SHP-2) in SIRPalpha1 activity. SHP-2 suppression resulted in a blockade of SIRPalpha1-mediated inhibition of anchorage-independent growth. Notably, we found that SIRPalpha1 did not act in v-Src-transformed cells by triggering cell growth arrest but by eliciting a suspension-selective apoptosis (anoikis), and that SHP-2 was required for this effect. Furthermore, we found that SHP-2 was crucial for recovery of stress fiber and focal contact formation by SIRPalpha1 in v-Src-transformed cells. Finally, we found that SIRPalpha1/SHP-2 signaling regulates anoikis in human breast carcinoma cells with activated c-Src. Taken together, our findings define SHP-2 as an essential component of tumor suppression and anoikis mediated by SIRPalpha1 in human breast carcinoma cells as well as in v-Src-transformed cells. |
| Dual faces of SH2-containing protein-tyrosine phosphatase Shp2/PTPN11 in tumorigenesis. | PTPN11, which encodes tyrosine phosphatase Shp2, is a critical gene mediating cellular responses to hormones and cytokines. Against original prediction as tumor suppressor for tyrosine phosphatases, PTPN11 was first identified as a proto-oncogene because activating mutations of this gene are associated with leukemogenesis. However, most recent experimental data suggest PTPN11/Shp2 acting as a tumor suppressor in hepatocarcinogenesis. This review focuses on the tumor-promoting or suppressing roles of the gene PTPN11/Shp2 in different cell types. |