CD151 promotes cell metastasis via activating TGF-β1/Smad signaling in renal cell carcinoma
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Yajie Yu1,*, Chao Liang1,*, Shangqian Wang1,*, Jundong Zhu1, Chenkui Miao1, Yibo Hua1, Meiling Bao2, Qiang Cao1, Chao Qin1, Pengfei Shao1 and Zengjun Wang1
1Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China
2Department of Pathology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China
*These authors have contributed equally to this work
Pengfei Shao, email: firstname.lastname@example.org
Qiang Cao, email: email@example.com
Keywords: CD151; epithelial-to-mesenchymal transition; metastasis; renal cell carcinoma; TGF-β1/Smad
Received: July 17, 2017 Accepted: January 02, 2018 Published: January 08, 2018
Tetraspanin CD151 has been identified as a tumor promoter, which is upregulated in various malignant cell types. However, the function of CD151 and its underlying mechanism in renal cell carcinoma is still unknown. In this study, we detected the expression of CD151 in RCC cells and tissues and explored its regulatory mechanism. We found that CD151 was upregulated in renal cell carcinoma tissues and cells and its expression was significantly associated with tumor stage (p=0.019) and survival (p=0.001) by analyzing tissue microarrays. After silencing of CD151 via lentivirus vector in Caki-1 and Caki-2 cells, reduced ability of migration and invasion were detected with downregulation of CD151. The opposite results were observed in cells with CD151 overexpression. Furthermore, western blotting was performed to investigate the influence of CD151 on epithelial-to-mesenchymal transition, matrix metalloproteinase 9 and TGF-β1/Smad signaling pathway in RCC. Subsequently, upregulating the protein level of transforming growth factor-β1 in cells with silencing of CD151 could rescue the malignant behaviors inhibited, which indicated that CD151 may play its promoting role in RCC partially by stimulating the expression of TGF-β1. Conclusively, CD151 might exhibit a prominent role in migration and invasion of RCC cells via activating TGF-β1/Smad signaling pathway.
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