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

Xiaoru Xin1, Yanan Lu1, Sijie Xie1

  • 1Shanghai Putuo District People's Hospital, School of Life Science and Technology, Tongji University, Shanghai 200092, China.

Molecular Therapy Oncolytics
|June 4, 2020
PubMed

Insights

MicroRNA 155 (miR-155) promotes liver cancer by inhibiting P21 expression through epigenetic changes. Restoring P21WAF1/Cip1 levels can counteract miR-155

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Research

Background:

  • MicroRNA 155 (miR-155) is implicated in promoting tumorigenesis.
  • A negative correlation exists between miR-155 expression and P21WAF1/Cip1 levels in liver cancer.

Purpose of the Study:

  • To elucidate the role of miR-155 in liver cancer development.
  • To investigate the molecular mechanisms by which miR-155 influences gene expression and epigenetic modifications.

Main Methods:

  • Analysis of miR-155 and P21WAF1/Cip1 expression.
  • Transcriptome alteration studies in liver cancer cells.
  • Investigation of histone methylation and protein phosphorylation modifications.
  • Assessment of RNA polymerase II binding to the P21WAF1/CIP1 promoter.

Main Results:

  • miR-155 inhibits H3F3A expression, leading to reduced methylation of histone H3 at lysine 27.
  • miR-155 promotes CDK2-cyclin E interaction and CDK2 phosphorylation by inhibiting H3F3A.
  • miR-155 blocks RNA polymerase II binding to the P21WAF1/CIP1 promoter, reducing P21WAF1/CIP1 transcription and translation.
  • Elevated P21WAF1/Cip1 expression counteracts the oncogenic functions of miR-155.

Conclusions:

  • miR-155 promotes liver cancer progression via epigenetic regulation of gene expression.
  • The miR-155/H3F3A/CDK2/P21WAF1/CIP1 axis is a key pathway in liver tumorigenesis.
  • Targeting miR-155 or restoring P21WAF1/Cip1 may offer therapeutic strategies for liver cancer.
Keywords:
CDK2H3F3AP21WAF1/Cip1liver cancermiR-155

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