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Long non-coding RNA SNHG5 suppresses gastric cancer progression by trapping MTA2 in the cytosol

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Abstract

Recently, intriguing new roles for some small nucleolar RNA host genes (SNHGs) in cancer have emerged. In the present study, a panel of SNHGs was profiled to detect aberrantly expressed SNHGs in gastric cancer (GC). The expression of SNHG5 was significantly downregulated in GC and was significantly associated with the formation of a tumor embolus and with the tumor, node and metastasis stage. SNHG5 was a long non-coding RNA, which was a class of non-coding RNA transcripts longer than 200 nucleotides. SNHG5 suppressed GC cell proliferation and metastasis in vitro and in vivo. Furthermore, SNHG5 exerted its function through interacting with MTA2, preventing the translocation of MTA2 from the cytoplasm into the nucleus. SNHG5 overexpression led to significant increases in the acetylation levels of histone H3 and p53, indicating that SNHG5 might affect acetylation by trapping MTA2 in the cytosol, thereby interfering with the formation of the nucleosome remodeling and histone deacetylation complex. This study is the first to demonstrate that SNHG5 is a critical and powerful regulator that is involved in GC progression through trapping MTA2 in the cytosol. These results imply that SNHG5 may be a novel therapeutic target for the treatment of GC.

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Acknowledgements

This work was partially supported by the State Key Basic Research Program of China (Grant No. 2013CB530805, to J Shi and D Zheng), the Natural Science Foundation of China (Grant No. 81372200, 81572755, to J Shi), the PUMC Youth Fund and the Fundamental Research Funds for the Central Universities (Grant No. 3332013055 and 3332014007, to J Shi).

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Correspondence to J Shi or D Zheng.

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Zhao, L., Guo, H., Zhou, B. et al. Long non-coding RNA SNHG5 suppresses gastric cancer progression by trapping MTA2 in the cytosol. Oncogene 35, 5770–5780 (2016). https://doi.org/10.1038/onc.2016.110

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