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Monoacylglycerol Lipase Knockdown Inhibits Cell Proliferation and Metastasis in Lung Adenocarcinoma

Abnormal metabolism is one of the hallmarks of cancer cells. Monoacylglycerol lipase (MGLL), a key enzyme in lipid metabolism, has emerged as an important regulator of tumor progression. In this study, we aimed to characterize the role of MGLL in the development of lung adenocarcinoma (LUAD). To thi...

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Autores principales: Zhang, Hao, Guo, Wei, Zhang, Fan, Li, Renda, Zhou, Yang, Shao, Fei, Feng, Xiaoli, Tan, Fengwei, Wang, Jie, Gao, Shugeng, Gao, Yibo, He, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7756122/
https://www.ncbi.nlm.nih.gov/pubmed/33363004
http://dx.doi.org/10.3389/fonc.2020.559568
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author Zhang, Hao
Guo, Wei
Zhang, Fan
Li, Renda
Zhou, Yang
Shao, Fei
Feng, Xiaoli
Tan, Fengwei
Wang, Jie
Gao, Shugeng
Gao, Yibo
He, Jie
author_facet Zhang, Hao
Guo, Wei
Zhang, Fan
Li, Renda
Zhou, Yang
Shao, Fei
Feng, Xiaoli
Tan, Fengwei
Wang, Jie
Gao, Shugeng
Gao, Yibo
He, Jie
author_sort Zhang, Hao
collection PubMed
description Abnormal metabolism is one of the hallmarks of cancer cells. Monoacylglycerol lipase (MGLL), a key enzyme in lipid metabolism, has emerged as an important regulator of tumor progression. In this study, we aimed to characterize the role of MGLL in the development of lung adenocarcinoma (LUAD). To this end, we used tissue microarrays to evaluate the expression of MGLL in LUAD tissue and assessed whether the levels of this protein are correlated with clinicopathological characteristics of LUAD. We found that the expression of MGLL is higher in LUAD samples than that in adjacent non-tumor tissues. In addition, elevated MGLL expression was found to be associated with advanced tumor progression and poor prognosis in LUAD patients. Functional studies further demonstrated that stable short hairpin RNA (shRNA)-mediated knockdown of MGLL inhibits tumor proliferation and metastasis, both in vitro and in vivo, and mechanistically, our data indicate that MGLL regulates Cyclin D1 and Cyclin B1 in LUAD cells. Moreover, we found that knockdown of MGLL suppresses the expression of matrix metalloproteinase 14 (MMP14) in A549 and H322 cells, and in clinical samples, expression of MMP14 is significantly correlated with MGLL expression. Taken together, our results indicate that MGLL plays an oncogenic role in LUAD progression and metastasis and may serve as a potential biomarker for disease prognosis and as a target for the development of personalized therapies.
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spelling pubmed-77561222020-12-24 Monoacylglycerol Lipase Knockdown Inhibits Cell Proliferation and Metastasis in Lung Adenocarcinoma Zhang, Hao Guo, Wei Zhang, Fan Li, Renda Zhou, Yang Shao, Fei Feng, Xiaoli Tan, Fengwei Wang, Jie Gao, Shugeng Gao, Yibo He, Jie Front Oncol Oncology Abnormal metabolism is one of the hallmarks of cancer cells. Monoacylglycerol lipase (MGLL), a key enzyme in lipid metabolism, has emerged as an important regulator of tumor progression. In this study, we aimed to characterize the role of MGLL in the development of lung adenocarcinoma (LUAD). To this end, we used tissue microarrays to evaluate the expression of MGLL in LUAD tissue and assessed whether the levels of this protein are correlated with clinicopathological characteristics of LUAD. We found that the expression of MGLL is higher in LUAD samples than that in adjacent non-tumor tissues. In addition, elevated MGLL expression was found to be associated with advanced tumor progression and poor prognosis in LUAD patients. Functional studies further demonstrated that stable short hairpin RNA (shRNA)-mediated knockdown of MGLL inhibits tumor proliferation and metastasis, both in vitro and in vivo, and mechanistically, our data indicate that MGLL regulates Cyclin D1 and Cyclin B1 in LUAD cells. Moreover, we found that knockdown of MGLL suppresses the expression of matrix metalloproteinase 14 (MMP14) in A549 and H322 cells, and in clinical samples, expression of MMP14 is significantly correlated with MGLL expression. Taken together, our results indicate that MGLL plays an oncogenic role in LUAD progression and metastasis and may serve as a potential biomarker for disease prognosis and as a target for the development of personalized therapies. Frontiers Media S.A. 2020-12-09 /pmc/articles/PMC7756122/ /pubmed/33363004 http://dx.doi.org/10.3389/fonc.2020.559568 Text en Copyright © 2020 Zhang, Guo, Zhang, Li, Zhou, Shao, Feng, Tan, Wang, Gao, Gao and He 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
Zhang, Hao
Guo, Wei
Zhang, Fan
Li, Renda
Zhou, Yang
Shao, Fei
Feng, Xiaoli
Tan, Fengwei
Wang, Jie
Gao, Shugeng
Gao, Yibo
He, Jie
Monoacylglycerol Lipase Knockdown Inhibits Cell Proliferation and Metastasis in Lung Adenocarcinoma
title Monoacylglycerol Lipase Knockdown Inhibits Cell Proliferation and Metastasis in Lung Adenocarcinoma
title_full Monoacylglycerol Lipase Knockdown Inhibits Cell Proliferation and Metastasis in Lung Adenocarcinoma
title_fullStr Monoacylglycerol Lipase Knockdown Inhibits Cell Proliferation and Metastasis in Lung Adenocarcinoma
title_full_unstemmed Monoacylglycerol Lipase Knockdown Inhibits Cell Proliferation and Metastasis in Lung Adenocarcinoma
title_short Monoacylglycerol Lipase Knockdown Inhibits Cell Proliferation and Metastasis in Lung Adenocarcinoma
title_sort monoacylglycerol lipase knockdown inhibits cell proliferation and metastasis in lung adenocarcinoma
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7756122/
https://www.ncbi.nlm.nih.gov/pubmed/33363004
http://dx.doi.org/10.3389/fonc.2020.559568
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