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Down-regulation of β3-integrin inhibits bone metastasis of small cell lung cancer

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Abstract

Bone is one of the most frequent targets of small cell lung cancer (SCLC) metastasis, but the molecular mechanism remains unclear. β3-integrin plays an important role in invasion of various kinds of tumors. Yet, its role in bone-metastasis of SCLC is still unknown. In this study, we first examined the expression of β3-integrin in SBC-5 and SBC-3 cells by real-time PCR, western blot and immunofluorescence. We found that, compared to none bone-metastatic SBC-3 cells, β3-integrin was highly expressed in SBC-5 cells, a specific bone-metastatic SCLC cells line characterized in our previous study. We next constructed β3-integrin siRNA and transfected SBC-5 cell line, and found that β3-integrin siRNA significantly down-regulated the β3-integrin mRNA level and protein expression in SBC-5 cell line. We further found that inhibition of β3-integrin significantly reduced tumor cell proliferation and induced apoptosis. In addition, the β3-integrin down-regulated cells presented significant decrease in cell adhesion, migration and invasion activity. Our results suggest the β3-integrin has an essential effect on tumor cell proliferation and progression, and may be a potential therapeutic target for the prevention of skeletal metastases of lung cancer.

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Acknowledgments

We thank Professor Sone (Third Department of Internal Medicine, University of Tokushima, Japan) for his generous gift of cell lines, and Jun-lei Zhang (Department of Microbiology, The Third Military Medical University, China) for his excellent technical assistance for the plasmid about Human β3-integrin-siRNA. This work was supported by grants from the National Natural Science Foundation of China (30873028) and from Foundation of Chinese Society of Clinical Oncology.

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Correspondence to He-long Zhang.

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Na Li and Jian-ping Zhang contributed equally to this work.

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Li, N., Zhang, Jp., Guo, S. et al. Down-regulation of β3-integrin inhibits bone metastasis of small cell lung cancer. Mol Biol Rep 39, 3029–3035 (2012). https://doi.org/10.1007/s11033-011-1065-y

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  • DOI: https://doi.org/10.1007/s11033-011-1065-y

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