OncoTargets and Therapy (Sep 2017)

Clinical significance of SLP-2 in hepatocellular carcinoma tissues and its regulation in cancer cell proliferation, migration, and EMT

  • Huang Y,
  • Chen Y,
  • Lin X,
  • Lin Q,
  • Han M,
  • Guo G

Journal volume & issue
Vol. Volume 10
pp. 4665 – 4673

Abstract

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Yijie Huang,1,* Yexi Chen,2,* Xiaoqi Lin,2 Qingjun Lin,2 Ming Han,2 Guohu Guo2 1Department of General Surgery, Guangdong General Hospital, Guangzhou, 2Department of General Surgery, The Second Affiliated Hospital of Shantou University Medical College, Shantou, People’s Republic of China *These authors contributed equally to this work Abstract: Stomatin-like protein 2 (SLP-2) gene was significantly upregulated in a variety of tumor tissues and found to be involved in proliferation and metastasis. However, its functional role in hepatocellular carcinoma (HCC) remains unknown. Our study was to investigate the function of SLP-2 in cell proliferation, migration, invasion, cell apoptosis, and the process of epithelial–mesenchymal transition (EMT) in HCC. SLP-2 mRNA and protein expression in HCC were assessed by qRT-PCR and immunohistochemical staining. In vitro, we determined cell proliferation, migration, invasion, and cell apoptosis by CCK-8, transwell, and flow cytometry assays, respectively. SLP-2 was found to be upregulated at both mRNA and protein levels in HCC tissues, and its aberrant overexpression was linked with poor prognosis in patients with HCC. SLP-2 downregulation by siRNAs significantly suppressed cell proliferation, migration, invasion, anti-apoptosis abilities, and inhibited EMT process in vitro. In conclusion, the present study demonstrated the overexpression of SLP-2 in HCC tissues for the first time. As an effective regulator involved in cell proliferation, migration, invasion, cell apoptosis, and EMT, SLP-2 could be a novel therapeutic target for patients with HCC who express high levels of SLP-2. Keywords: hepatocellular carcinoma, stomatin-like protein 2, prognosis, proliferation, migration, epithelial–mesenchymal transition 

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