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Licensed Unlicensed Requires Authentication Published by De Gruyter July 16, 2020

Histone deacetylase 1 regulates the malignancy of oral cancer cells via miR-154-5p/PCNA axis

  • Yuanjing Lv , Jinle Lu , Xin Liu , Susheng Miao , Xionghui Mao , Baojun Li , Rong Pei EMAIL logo and Cheng Xiang EMAIL logo
From the journal Biological Chemistry

Abstract

Histone deacetylases (HDACs) can regulate the progression of various cancers, while their roles in oral cancer cells are not well known. Our present study found that the HDAC1 was over expressed in oral squamous cell carcinoma (OSCC) cells and tissues. Targeted inhibition of HDAC1 via its specific inhibitor PCI24781 or siRNA can inhibit the proliferation of OSCC cells and increase their sensitivity to the chemo-sensitivity such as doxorubicin treatment. HDAC1 can regulate the expression of proliferating cell nuclear antigen (PCNA) via decreasing its mRNA stability. While over expression of PCNA can attenuate HDAC1 inhibition induced suppression of cell proliferation. We checked the expression of various miRNAs which can target the 3′UTR of PCNA. Results showed that HDAC1 can negative regulate the expression of miR-154-5p, inhibitor of miR-154-5p can attenuate PCI24781 treatment decreased PCNA expression and cell proliferation. Collectively, our present study suggested that HDAC1 can promote the growth and progression of OSCC via regulation of miR-154-5p/PCNA signals.


Corresponding authors: Rong Pei, Department of Head and Neck Surgery, Harbin Medical University Cancer Hospital, Harbin 150040, China, E-mail: ; and Cheng Xiang, Department of Head and Neck Surgery, Harbin Medical University Cancer Hospital, Harbin 150040, China, E-mail: .
Yuanjing Lv and Jinle Lu: These authors contributed equally to this work.

Award Identifier / Grant number: LBH-Z18145

  1. Author contribution: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  2. Research funding: This work was supported by the Heilongjiang Postdoctoral Fund (LBH-Z18145).

  3. Ethics approval and consent to participate, consent for publication: The approval to conduct this study was obtained from the Ethical Committee in our hospital. All patients were obtained with written informed consent signed by the donors voluntarily for research with no financial payment. All data and material are available upon request.

  4. Conflict of interest statement: The authors declare no conflict of interest.

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Received: 2020-01-04
Accepted: 2020-06-01
Published Online: 2020-07-16
Published in Print: 2020-10-25

© 2020 Walter de Gruyter GmbH, Berlin/Boston

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