Статья

miR-155 Accelerates the Growth of Human Liver Cancer Cells by Activating CDK2 via Targeting H3F3A

Xiaoru XinShanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, ChinaYanan LuShanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, ChinaSijie XieShanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, ChinaYing‐Jie ChenShanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, ChinaXiaoxue JiangShanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, ChinaShuting SongShanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, ChinaLiyan WangShanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, ChinaPu HuShanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, ChinaXin GuiShanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, ChinaTianming LiShanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, ChinaJie XuSchool of Medicine, Tongji University, Shanghai 200092, ChinaJiao LiSchool of Medicine, Tongji University, Shanghai 200092, ChinaSong JiaSchool of Medicine, Tongji University, Shanghai 200092, ChinaDongdong LuShanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, China

2020en

ABI

Аннотация

miR-155 is associated with the promotion of tumorigenesis. Herein, we indicate that abnormal miR-155 was negatively correlated with the expression of P21WAF1/Cip1. Our results suggest that miR-155 alters the transcriptome and inhibits the expression of H3F3A in liver cancer cells. Therefore, miR-155 inhibits the methylation modification of histone H3 on the 27th lysine. Notably, on the one hand, miR-155-dependent CTCF loops cause the CDK2 interacting with cyclin E in liver cancer cells; on the other hand, miR-155 promotes the phosphorylation modification of CDK2 by inhibiting H3F3A. Subsequently, miR-155 competitively blocks the binding of RNA polymerase II (RNA Pol II) to the P21WAF1/CIP1 promoter by increasing the phosphorylation of CDK2, inhibiting the transcription and translation of P21WAF1/CIP1. Strikingly, excessive P21WAF1/CIP1 abolishes the cancerous function of miR-155. In conclusion, miR-155 can play a positive role in the development of liver cancer and influence a series of gene expression through epigenetic regulation. miR-155 is associated with the promotion of tumorigenesis. Herein, we indicate that abnormal miR-155 was negatively correlated with the expression of P21WAF1/Cip1. Our results suggest that miR-155 alters the transcriptome and inhibits the expression of H3F3A in liver cancer cells. Therefore, miR-155 inhibits the methylation modification of histone H3 on the 27th lysine. Notably, on the one hand, miR-155-dependent CTCF loops cause the CDK2 interacting with cyclin E in liver cancer cells; on the other hand, miR-155 promotes the phosphorylation modification of CDK2 by inhibiting H3F3A. Subsequently, miR-155 competitively blocks the binding of RNA polymerase II (RNA Pol II) to the P21WAF1/CIP1 promoter by increasing the phosphorylation of CDK2, inhibiting the transcription and translation of P21WAF1/CIP1. Strikingly, excessive P21WAF1/CIP1 abolishes the cancerous function of miR-155. In conclusion, miR-155 can play a positive role in the development of liver cancer and influence a series of gene expression through epigenetic regulation.

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Идентификаторы

DOI: 10.1016/j.omto.2020.05.002

Цитирования и источники

Цитирований: 2Использованных источников: 0

Показатели — AkademScholar