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MGr1-Ag/37LRP promotes growth and proliferation of gastric cancer in vitro and in vivo

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Abstract

Gastric carcinoma (GC) is an aggressive cancer with a poor prognosis. We previously reported that MGr1-Ag was involved in multidrug resistance and anti-apoptosis in GC. However, the exact function of MGr1-Ag in GC proliferation is not clear. In this study, we found that MGr1-Ag was highly expressed in GC tissues and four GC cell lines compared with nontumor gastric tissues or gastric epithelial mucosa cells. The high expression of MGr1-Ag/37LRP was also consistent with the decreased median survival time of GC patients. We employed lenti-mediated RNA interference technique to knock down MGr1-Ag expression in SGC7901 and MKN45 cells, respectively, and observed its effects on GC cells growth in vitro and in vivo. Further study showed that knockdown of MGr1-Ag could inhibit GC cell proliferation by inhibiting the cell cycle S-phase entry and induced apoptosis. Soft agar colony formation assay indicated that the colony formation ability of SGC7901 and MKN45 cells decreased after lenti-MGr1-Ag small interfering RNA (siRNA) infection. Western blot revealed that cyclin D1 and Bcl-2 expression were downregulated whereas p27 and Bax were upregulated in lenti-MGr-siRNA-infected GC cells. Further study demonstrated that the proliferation effect of MGr1-Ag in GC is dependent on its laminin-binding region. Taken together, these data revealed a novel function of MGr1-Ag that can possibly be used as an independent prognostic factor and a potential therapeutic target for GC.

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Acknowledgements

This study was supported by Grants (no. 81101765 and no. 81272349) from the National Nature Science Foundation of China.

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Correspondence to H Zhang.

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Liu, L., Sun, L., Wu, K. et al. MGr1-Ag/37LRP promotes growth and proliferation of gastric cancer in vitro and in vivo. Cancer Gene Ther 21, 355–363 (2014). https://doi.org/10.1038/cgt.2014.36

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  • DOI: https://doi.org/10.1038/cgt.2014.36

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