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©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
Depletion of MRPL35 inhibits gastric carcinoma cell proliferation by regulating downstream signaling proteins
Ling Yuan, Jia-Xin Li, Yi Yang, Yan Chen, Ting-Ting Ma, Shuang Liang, Yang Bu, Lei Yu, Yi Nan
Ling Yuan, Jia-Xin Li, Yi Yang, Ting-Ting Ma, Pharmacy College of Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
Ling Yuan, Yi Nan, Key Laboratory of Hui Ethnic Medicine Modernization of Ministry of Education, Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
Yan Chen, Traditional Chinese Medicine College, Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
Shuang Liang, Department of Oncology and Endocrinology, Yinchuan Hospital of Traditional Chinese Medicine Affiliated to Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
Yang Bu, Department of Hepatobiliary Surgery, General Hospital of Ningxia Medical University, Yinchuan 750004, Ningxia Hui Autonomous Region, China
Lei Yu, Department of Infectious Diseases, The Fourth Hospital of Harbin Medical University, Harbin 150001, Heilongjiang Province, China
Author contributions: Nan Y provided the conceptual and technical guidance, designed the study, and revised the manuscript critically for important intellectual content; Yuan L carried out most of in vivo studies, analyzed the data, and wrote the manuscript; Li JX carried out all of in vitro experiments and wrote the manuscript; Yang Y and Ma TT performed parts of in vivo studies; Chen Y conducted statistical analysis of all of the data; Liang S, Bu Y, and Yu L supervised the clinical relevance and coordinated the clinic pathological features; all authors have read and approved the manuscript.
Supported by Ningxia Natural Science Foundation, No. 2020AAC03130.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board of Ningxia Medical University (No. 2020-071).
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Ningxia Medical University (IACUC protocol number: 2019-083).
Conflict-of-interest statement: All authors declare no financial or commercial conflict of interest.
Data sharing statement: All data generated or analyzed during this study are included in this published article.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
http://creativecommons.org/Licenses/by-nc/4.0/ Corresponding author: Yi Nan, MD, PhD, Professor, Key Laboratory of Hui Ethnic Medicine Modernization of Ministry of Education, Ningxia Medical University, No. 1160 Shengli Street, Yinchuan 750004, Ningxia Hui Autonomous Region, China. 20080011@nxmu.edu.cn
Received: December 22, 2020
Peer-review started: December 22, 2020
First decision: January 23, 2021
Revised: February 4, 2021
Accepted: March 11, 2021
Article in press: March 11, 2021
Published online: April 28, 2021
ARTICLE HIGHLIGHTS
Research background
Gastric carcinoma (GC) is one of the most common cancers, and the existing treatment methods cannot meet the treatment needs for GC. At the same time, MRPL35, a member of the large subunit family of mitochondrial ribosomal protein, shows the characteristics of oncogene in certain cancers.
Research motivation
The existing treatment methods for GC mainly include drugs, chemotherapy, and surgery, all of which have certain defects. Finding new therapeutic targets will be of great benefit to patients with GC.
Research objectives
The present study aimed to explore the correlation between MRPL35 and GC, and the effect of knockdown of MRPL35 on GC cells.
Research methods
The expression of MRPL35 in GC and the effect of MRPL35 on the prognosis of GC were evaluated based on data from public databases. Immunohistochemistry staining and pathological factors analysis were performed on 64 pairs of GC tissues and matched adjacent tissues. The effect of MRPL35 on the proliferation and apoptosis of GC cells was determined by Celigo cell count assay, flow cytometry, and tumor formation experiment in BABL/c nude mice. The related proteins that changed after knockdown of MRPL35 was identified by proteomic analysis and tested by Western blot.
Research results
The expression of MRPL35 was up-regulated in GC and high expression of MRPL35 was associated with a poor survival in GC. The expression of MRPL35 in GC tissues was increased in comparison with matched adjacent tissues, which was related to age, lymph node metastasis, and pathological tumor-node-metastasis stage. Knockdown of MRPL35 inhibited GC cell proliferation and colony formation and induced apoptosis. After knockdown of MRPL35, the expression of PICK1 and BCL-XL protein decreased, and that of AGR2 protein increased.
Research conclusions
MRPL35 is up-regulated in GC, and knockdown of MRPL35 could inhibit the proliferation of GC cells and induce apoptosis.
Research perspectives
MRPL35 can be used for targeted therapy of GC, and can also be used as a new biomarker for GC.
