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MicroRNA-155 Suppresses the Translation of p38 and Impairs the Functioning of Dendritic Cells in Endometrial Cancer Mice

Authors Jia J, Li X, Guo S, Xie X

Received 3 December 2019

Accepted for publication 31 March 2020

Published 30 April 2020 Volume 2020:12 Pages 2993—3002

DOI https://doi.org/10.2147/CMAR.S240926

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Antonella D'Anneo


Jianjun Jia,1 Xiaomao Li,2 Suiqun Guo,3 Xingmei Xie1

1Department of Obstetrics and Gynecology, The First Affiliated Hospital, Jinan University, Guangzhou 510632, People’s Republic of China; 2Department of Obstetrics and Gynecology, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510632, People’s Republic of China; 3Department of Obstetrics and Gynecology, The Third Affiliated Hospital, Southern Medical University, Guangzhou 510632, People’s Republic of China

Correspondence: Jianjun Jia
Department of Obstetrics and Gynecology, The First Affiliated Hospital, Jinan University, Guangzhou 510632, People’s Republic of China
Tel/ Fax +86-020-38688359
Email jiajianjun615@sohu.com

Background: Dendritic cells (DCs) are reported to play an important role in activating the anti-tumor immune responses. p38 MAPK14 signaling plays an important role in controlling their activity. Here, we identified that miR-155 suppressed the translation of p38 and impaired the functioning of dendritic cells in endometrial cancer.
Methods: HEC1A endometrial cancer cell lines were used for the study which was transfected in the C57BL/6 mice. Murine bone marrow-derived dendritic cells (BMDCs) were isolated from the mice. Target prediction was done by TargetScan which was confirmed by RT-PCR analysis. The protein expression was carried by Western blot analysis. Levels of IL-12 were evaluated by ELISA. Mice injected with HEC1A cells were subjected to tumor challenge study.
Results: On screening the binding sites of p38 MAPK14 gene, miR-155 was found to bind the 3ʹUTR directly and blocked its translation. The levels of miR-155 were upregulated in dendritic cells and RAW264.7 cells, miR-155 showed inhibitory effect on expression levels of p38. In dendritic cells, miR-155 was found to regulate the expression of IL-12, also miR-155 inhibitor stimulated the differentiation of Th1 cells in mice induced with endometrial cancer. In dendritic cells, miR-155 inhibited the expression of p38 gene and decreased their ability to interfere in tumor growth.
Conclusion: The study concludes suppressive role of miR-155 in the process of dendritic cells mediated anti-tumor immunity, also inhibiting miR-155 provides a novel strategy for countering endometrial cancer.

Keywords: miR-155, dendritic cells, p38, IL-12, RAW264.7 cells

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