Serine-arginine protein kinase 1 (SRPK1) is elevated in gastric cancer and plays oncogenic functions
Metrics: PDF 871 views | HTML 1650 views | ?
Xiaotao Xu1, Yuehua Wei1, Shidong Wang1, Man Luo1 and Heng Zeng2
1Department of Oncology, Renmin Hospital, Wuhan University, Wuhan, Hubei, 430060, China
2Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, China
Heng Zeng, email: firstname.lastname@example.org
Keywords: gastric adenocarcinoma, invasion, prognosis, proliferation, SRPK1
Received: April 15, 2017 Accepted: May 23, 2017 Published: June 28, 2017
Serine-arginine protein kinase 1 (SRPK1) phosphorylates proteins involved in the regulation of several mRNA processing pathways including alternative splicing. SRPK1 has been reported to be over-expressed in multiple cancers including prostate, breast, lung and glioma. Several studies further identified that inhibition of SRPK1 showed tumor-suppressive effects, thus raising SRPK1 as a novel candidate chemotherapy target. Interestingly, SRPK1 plays tumor suppressing role in mouse embryonic fibroblasts, on that SRPK1-silencing induces cell transformation. Therefore, the effect of SRPK1 seems heterogeneously in different cell types and tissues. The existence and role of SRPK1 in gastric cancer (GC) hasn’t been reported. Here we investigated the expression pattern of SRPK1 in GC by immunohistochemistry and found that it was up-regulated in tumor tissues, where its expression was correlated with tumor grade and prognosis. Further, we explored the signaling mechanism of SRPK1 in promoting GC progression, which revealed that both PP2A and DUSP6 phosphatases impaired the oncogenic effects of SRPK1. However, we didn’t find any direct interaction between SRPK1 with PP2A or DUSP6, indicating PP2A and DUSP6 function by regulating the downstream effectors of SRPK1. Our study not only revealed the clinical significance of SRPK1 in GC, but also provided new evidence for its signaling modulation which is invaluable for novel chemotherapy development.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.