Abstract
The Src homology 2 (SH2) domain-containing protein tyrosine phosphatase 1 (SHP-1), a non-receptor protein tyrosine phosphatase, has been reported as a negative regulator of phosphorylated signal transducer and activator of transcription 3 (STAT3) and linked to tumor development. In this present review, we will discuss the importance and function of SHP-1/p-STAT3 signaling in nonmalignant conditions as well as malignancies, its cross-talk with other pathways, the current clinical development and the potential role of inhibitors of this pathway in anticancer therapy and clinical relevance of SHP-1/p-STAT3 in cancers. Lastly, we will summarize and highlight work involving novel drugs/compounds targeting SHP-1/p-STAT3 signaling and combined strategies that were/are discovered in our and our colleagues’ laboratories.
Highlights
Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor which functions mainly through dimerization upon phosphorylation at tyrosine residues and translocation to cell nuclei [1,2]
We proved that sorafenib and its analogues SC-1 and SC-43 showed no obvious effects on the phosphorylation of signal transducer and activator of transcription 3 (STAT3) upstream regulator JAK1 or JAK2, but effectively decreased the p-STAT3 proteins [68]
Loss of SHP-1 contributes to the activation of Janus associated kinase (JAK)/STAT3 as well as the other oncogenic pathways, and may further spark off an oncogenic feedforward loop to amplify tumorigenic signals
Summary
Alteration of SHP-1/p-STAT3 Signaling: A Potential Target for Anticancer Therapy. Tzu-Ting Huang 1,2, Jung-Chen Su 3,4, Chun-Yu Liu 1,2,5,*, Chung-Wai Shiau 3,* and Kuen-Feng Chen 6,7,*. Academic Editor: Terrence Piva Received: 2 May 2017; Accepted: 5 June 2017; Published: 8 June 2017
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