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MRPS30-DT Knockdown Inhibits Breast Cancer Progression by Targeting Jab1/Cops5

Longnoncoding RNAs (lncRNAs) are significantly correlated with cancer pathogenesis, development, and metastasis. Microarray analysis showed that lncRNA MRPS30-DT is overexpressed in breast carcinoma; however, the function of MRPS30-DT in breast cancer tumorigenesis remains unclear. In situ hybridiza...

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Autores principales: Wu, Balu, Pan, Yunbao, Liu, Guohong, Yang, Tian, Jin, Yanxia, Zhou, Fuling, Wei, Yongchang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6854119/
https://www.ncbi.nlm.nih.gov/pubmed/31788446
http://dx.doi.org/10.3389/fonc.2019.01170
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author Wu, Balu
Pan, Yunbao
Liu, Guohong
Yang, Tian
Jin, Yanxia
Zhou, Fuling
Wei, Yongchang
author_facet Wu, Balu
Pan, Yunbao
Liu, Guohong
Yang, Tian
Jin, Yanxia
Zhou, Fuling
Wei, Yongchang
author_sort Wu, Balu
collection PubMed
description Longnoncoding RNAs (lncRNAs) are significantly correlated with cancer pathogenesis, development, and metastasis. Microarray analysis showed that lncRNA MRPS30-DT is overexpressed in breast carcinoma; however, the function of MRPS30-DT in breast cancer tumorigenesis remains unclear. In situ hybridization and immunohistochemical analysis were used to evaluate the expression levels of MRPS30-DT and Jab1 in clinical samples of breast carcinoma and their relation to survival outcome. qRT-PCR was used to measure MRPS30-DT and Jab1 mRNA expressions. Protein levels were detected using Western blot. Cell proliferation and invasion ability were evaluated via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, and transwell assays. MRPS30-DT was knocked down in breast cancer cells to investigate its potential functional roles in cell growth and metastasis in vitro and in vivo. We found that MRPS30-DT was upregulated in breast cancer specimens and was accompanied by high Jab1 expression compared with that of paired para-carcinoma tissues. Knocking down MRPS30-DT significantly inhibited cancer cell proliferation and invasion and induced apoptosis in breast cancer cells. Similarly, knocking down MRPS30-DT in MDA-MB-231 cells significantly suppressed tumor growth. Furthermore, knocking down MRPS30-DT markedly reduced Jab1 expression in breast cancer cells and murine carcinoma. Statistical analyses suggested that high MRPS30-DT or Jab1 levels in breast cancer patients were positively correlated with poor prognoses. These data indicate the possible mechanisms of MRPS30-DT and Jab1 in breast cancer; thus, MRPS30-DT and Jab1 may be novel prognostic biomarkers and potential therapeutic targets for breast cancer treatment.
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spelling pubmed-68541192019-11-29 MRPS30-DT Knockdown Inhibits Breast Cancer Progression by Targeting Jab1/Cops5 Wu, Balu Pan, Yunbao Liu, Guohong Yang, Tian Jin, Yanxia Zhou, Fuling Wei, Yongchang Front Oncol Oncology Longnoncoding RNAs (lncRNAs) are significantly correlated with cancer pathogenesis, development, and metastasis. Microarray analysis showed that lncRNA MRPS30-DT is overexpressed in breast carcinoma; however, the function of MRPS30-DT in breast cancer tumorigenesis remains unclear. In situ hybridization and immunohistochemical analysis were used to evaluate the expression levels of MRPS30-DT and Jab1 in clinical samples of breast carcinoma and their relation to survival outcome. qRT-PCR was used to measure MRPS30-DT and Jab1 mRNA expressions. Protein levels were detected using Western blot. Cell proliferation and invasion ability were evaluated via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, and transwell assays. MRPS30-DT was knocked down in breast cancer cells to investigate its potential functional roles in cell growth and metastasis in vitro and in vivo. We found that MRPS30-DT was upregulated in breast cancer specimens and was accompanied by high Jab1 expression compared with that of paired para-carcinoma tissues. Knocking down MRPS30-DT significantly inhibited cancer cell proliferation and invasion and induced apoptosis in breast cancer cells. Similarly, knocking down MRPS30-DT in MDA-MB-231 cells significantly suppressed tumor growth. Furthermore, knocking down MRPS30-DT markedly reduced Jab1 expression in breast cancer cells and murine carcinoma. Statistical analyses suggested that high MRPS30-DT or Jab1 levels in breast cancer patients were positively correlated with poor prognoses. These data indicate the possible mechanisms of MRPS30-DT and Jab1 in breast cancer; thus, MRPS30-DT and Jab1 may be novel prognostic biomarkers and potential therapeutic targets for breast cancer treatment. Frontiers Media S.A. 2019-11-07 /pmc/articles/PMC6854119/ /pubmed/31788446 http://dx.doi.org/10.3389/fonc.2019.01170 Text en Copyright © 2019 Wu, Pan, Liu, Yang, Jin, Zhou and Wei. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Oncology
Wu, Balu
Pan, Yunbao
Liu, Guohong
Yang, Tian
Jin, Yanxia
Zhou, Fuling
Wei, Yongchang
MRPS30-DT Knockdown Inhibits Breast Cancer Progression by Targeting Jab1/Cops5
title MRPS30-DT Knockdown Inhibits Breast Cancer Progression by Targeting Jab1/Cops5
title_full MRPS30-DT Knockdown Inhibits Breast Cancer Progression by Targeting Jab1/Cops5
title_fullStr MRPS30-DT Knockdown Inhibits Breast Cancer Progression by Targeting Jab1/Cops5
title_full_unstemmed MRPS30-DT Knockdown Inhibits Breast Cancer Progression by Targeting Jab1/Cops5
title_short MRPS30-DT Knockdown Inhibits Breast Cancer Progression by Targeting Jab1/Cops5
title_sort mrps30-dt knockdown inhibits breast cancer progression by targeting jab1/cops5
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6854119/
https://www.ncbi.nlm.nih.gov/pubmed/31788446
http://dx.doi.org/10.3389/fonc.2019.01170
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