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. 2016 Jun 27;5(6):e237. doi: 10.1038/oncsis.2016.24

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Copyright © 2016 Macmillan Publishers Limited

Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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The expression of RASSF10 and its promoter methylation status. (a) The expression profile of RASSF10 mRNA in HCC cell lines and normal liver tissue by RT-PCR. (b)The mRNA expression level of RASSF10 was significantly down-regulated in primary HCCs as compared with their adjacent normal tissues by quantitative real-time PCR (P=0.003, n=52). RASSF10 expression level was normalized with the GAPDH mRNA level. (c) Methylation-specific polymerase chain reaction showed methylation of RASSF10 in HCC cell lines. M, methylated DNA; U, unmethylated DNA. (d) BGS confirmed the methylation status of RASSF10 in HCC cell lines and normal control. (e) RASSF10 mRNA expression was restored following 5-aza-DC treatment. GAPDH was used as a control for equal loading.