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Targeting CD151 by lentivirus-mediated RNA interference inhibits luminal and basal-like breast cancer cell growth and invasion

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Abstract

CD151 is a member of the tetraspanin family, which is involved in diverse cellular processes, including proliferation, motility, and invasion. However, the role of CD151 in breast cancer especially luminal and basal-like subtype breast cancer remains obscure. Here, we report the role of CD151 in the biological behaviors of luminal and basal-like subtype cell lines and the underlying molecular mechanism. A eukaryotic expression vector expressing both CD151 shRNA and GFP was transfected into MCF-7 and MDA-MB-468 cells. The CD151 gene-silencing effect is authenticated by real-time PCR and Western blot. Our data show that the capacity for proliferation, migration, and invasion of two kinds of cells is diminished after Knockdown of CD151 via lentivirus-mediated CD151 specific shRNA. Tumor cells are arrested in G0/G1 phase. Apoptosis is increased. Moreover, we also demonstrate that the expressions of mmp26 and CD147 are inhibited by knockdown of CD151. But the inhibition depends on the cell type. We can conclude that silencing gene CD151 inhibits expression of properties that are associated with the malignant phenotype of MCF-7 and MDA-MB-468 cells. It may become a potential target in breast cancer therapy especially for luminal and basal subtypes.

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Acknowledgments

This work was supported by the Major State Basic Research Development Program of China (973 Program) (81172499), the project of Heilongjiang Education Department(11511453,12521626), The Science and Technology Development Fund of Jilin Province (20076023), and the platform foundation from Jilin University (450060445657).

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The authors declare that they have no conflict of interest.

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Correspondence to Yulin Li.

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Liu, T., wang, S., Wang, L. et al. Targeting CD151 by lentivirus-mediated RNA interference inhibits luminal and basal-like breast cancer cell growth and invasion. Mol Cell Biochem 407, 111–121 (2015). https://doi.org/10.1007/s11010-015-2459-2

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  • DOI: https://doi.org/10.1007/s11010-015-2459-2

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