caa a22 4500 60623571X CHVBK 20210128101244.0 cr unu---uuuuu 210128e20150901xx s 000 0 eng 10.1007/s11010-015-2459-2 doi (NATIONALLICENCE)springer-10.1007/s11010-015-2459-2 Targeting CD151 by lentivirus-mediated RNA interference inhibits luminal and basal-like breast cancer cell growth and invasion [Elektronische Daten] [Ting Liu, Shaoqing wang, Liping Wang, Junping Wang, Yulin Li] 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. Springer Science+Business Media New York, 2015 CD151 nationallicence Gene silencing nationallicence Breast cancer nationallicence Growth nationallicence Invasion nationallicence Liu Ting The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, Changchun, Jilin, China aut wang Shaoqing Department of Pathology, Qiqihar Medical University, Qiqihar, China aut Wang Liping Department of Pathology, Qiqihar Medical University, Qiqihar, China aut Wang Junping Department of Pathology, Qiqihar Medical University, Qiqihar, China aut Li Yulin The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, Changchun, Jilin, China aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 407/1-2(2015-09-01), 111-121 0300-8177 407:1-2<111 2015 407 11010 https://doi.org/10.1007/s11010-015-2459-2 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-015-2459-2 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Liu Ting The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, Changchun, Jilin, China aut NATIONALLICENCE 700 1- wang Shaoqing Department of Pathology, Qiqihar Medical University, Qiqihar, China aut NATIONALLICENCE 700 1- Wang Liping Department of Pathology, Qiqihar Medical University, Qiqihar, China aut NATIONALLICENCE 700 1- Wang Junping Department of Pathology, Qiqihar Medical University, Qiqihar, China aut NATIONALLICENCE 700 1- Li Yulin The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, Changchun, Jilin, China aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 407/1-2(2015-09-01), 111-121 0300-8177 407:1-2<111 2015 407 11010