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miR-148b Functions as a Tumor Suppressor by Targeting Endoplasmic Reticulum Metallo Protease 1 in Human Endometrial Cancer Cells

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* Department of Obstetrics and Gynecology, Jinan Central Hospital, Jinan, P.R. China
† Department of Obstetrics and Gynecology, Dongying People’s Hospital, Dongying, P.R. China

Oncology Research 2019, 27(1), 81-88. https://doi.org/10.3727/096504018X15202988139874

A retraction of this article was approved in:

Retraction: miR-148b Functions as a Tumor Suppressor by Targeting Endoplasmic Reticulum Metallo Protease 1 in Human Endometrial Cancer Cells
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Abstract

This study investigated the tumor-suppressive role of miR-148b in regulating endoplasmic reticulum metalloprotease 1 (ERMP1) expression and the oxidative stress response in endometrial cancer cells. Human endometrial cancer RL95-2 cells were used and transfected with miR-148b mimic, miR-148b inhibitor, or their scrambled negative control. Thereafter, the transfection efficiency was determined by RT-qPCR, and cell proliferation was assessed by MTT assay. The dual-luciferase reporter assay, Western blot, and RT-qPCR were conducted to determine the target gene of miR-148b. ERMP1 is a putative target of miR-148b, and thereby the overexpression and downregulation of ERMP1 on the proliferation of RL95-2 cells were assessed. Next, the expressions of hypoxia-inducible factor 1 (HIF-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) were analyzed by Western blot. Intracellular reactive oxygen species (ROS) was determined using dichlorofluorescin diacetate (DCFDA). Results showed that differential expression of miR-148b or ERMP1 was observed in normal endometrial tissues and endometrial cancerous tissues. Enhanced expression of miR-148b effectively inhibited proliferation of RL95-2 cells. ERMP1 was the target of miR-148b. ERMP1 silencing obviously suppressed proliferation of RL95-2 cells. Thus, miR-148b repressed cell proliferation, likely through downregulating ERMP1. Furthermore, it was observed that miR-148b significantly decreased expression of HIF-1 and Nrf2 by downregulating ERMP1. The intracellular ROS level was enhanced by miR-148b via downregulating ERMP1. To conclude, our results suggested that miR-148b suppressed cell proliferation and regulated the oxidative stress response in human endometrial cancer RL95-2 cells by inhibiting ERMP1.

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APA Style
Qu, J., Zhang, L., Li, L., Su, Y. (2019). Mir-148b functions as a tumor suppressor by targeting endoplasmic reticulum metallo protease 1 in human endometrial cancer cells. Oncology Research, 27(1), 81-88. https://doi.org/10.3727/096504018X15202988139874
Vancouver Style
Qu J, Zhang L, Li L, Su Y. Mir-148b functions as a tumor suppressor by targeting endoplasmic reticulum metallo protease 1 in human endometrial cancer cells. Oncol Res. 2019;27(1):81-88 https://doi.org/10.3727/096504018X15202988139874
IEEE Style
J. Qu, L. Zhang, L. Li, and Y. Su, “miR-148b Functions as a Tumor Suppressor by Targeting Endoplasmic Reticulum Metallo Protease 1 in Human Endometrial Cancer Cells,” Oncol. Res., vol. 27, no. 1, pp. 81-88, 2019. https://doi.org/10.3727/096504018X15202988139874



cc Copyright © 2019 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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