Negatively Regulated by miR-29c-3p, MTFR1 Promotes the Progression and Glycolysis in Lung Adenocarcinoma via the AMPK/mTOR Signalling Pathway

Background: Lung adenocarcinoma (LUAD) is the major form of lung cancer that presents a major peril to public health. Owing to the high rates of morbidity, mortality and chemoresistance, it is necessary to develop more effective therapeutic targets of LUAD. Mitochondrial fission regulator 1 (MTFR1)...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Yongmeng Li, Yanfei Liu, Kai Jin, Rui Dong, Cun Gao, Libo Si, Zitong Feng, Huiying Zhang, Hui Tian
Formato: article
Lenguaje:EN
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://doaj.org/article/9badcc4e38704b4abec3618eded133c8
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:9badcc4e38704b4abec3618eded133c8
record_format dspace
spelling oai:doaj.org-article:9badcc4e38704b4abec3618eded133c82021-12-02T00:36:30ZNegatively Regulated by miR-29c-3p, MTFR1 Promotes the Progression and Glycolysis in Lung Adenocarcinoma via the AMPK/mTOR Signalling Pathway2296-634X10.3389/fcell.2021.771824https://doaj.org/article/9badcc4e38704b4abec3618eded133c82021-12-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcell.2021.771824/fullhttps://doaj.org/toc/2296-634XBackground: Lung adenocarcinoma (LUAD) is the major form of lung cancer that presents a major peril to public health. Owing to the high rates of morbidity, mortality and chemoresistance, it is necessary to develop more effective therapeutic targets of LUAD. Mitochondrial fission regulator 1 (MTFR1) affects the occurrence and development of some diseases by regulating mitochondrial dynamics and is dysregulated in LUAD. However, the functions and molecular mechanisms of MTFR1 in LUAD have not been investigated.Methods: Immunohistochemical (IHC) analysis, real-time quantitative polymerase chain reaction (RT-qPCR), bioinformatic analysis and western blot (WB) were performed to assess the expression of MTFR1 at both protein and mRNA levels. The biological functions of MTFR1 in LUAD cells were assessed based on various in vivo and in vitro experiments. The dual-luciferase reporter assay and some rescue experiments were performed to evaluate the underlying mechanism of MTFR1 in LUAD.Results: MTFR1 was upregulated in LUAD cells and tissues and correlated with dismal clinicopathologic features and a worse prognosis of patients with LUAD. Functionally, MTFR1 overexpression stimulated the proliferation, invasion, migration and glycolytic capacity and impeded the apoptosis of LUAD cells; however, opposite results were obtained when MTFR1 expression was knocked down. MTFR1, which was directly targeted by miR-29c-3p, may exert its biological functions through the AMPK/mTOR signalling pathway.Conclusion: MTFR1 promotes the progression of LUAD. Therefore, targeting MTFR1 can offer an effective therapeutic strategy for LUAD treatment.Yongmeng LiYanfei LiuKai JinRui DongCun GaoLibo SiZitong FengHuiying ZhangHui TianFrontiers Media S.A.articlelung cancermicroRNAmitochondrial fission regulator 1Warburg effectproliferationinvasionBiology (General)QH301-705.5ENFrontiers in Cell and Developmental Biology, Vol 9 (2021)
institution DOAJ
collection DOAJ
language EN
topic lung cancer
microRNA
mitochondrial fission regulator 1
Warburg effect
proliferation
invasion
Biology (General)
QH301-705.5
spellingShingle lung cancer
microRNA
mitochondrial fission regulator 1
Warburg effect
proliferation
invasion
Biology (General)
QH301-705.5
Yongmeng Li
Yanfei Liu
Kai Jin
Rui Dong
Cun Gao
Libo Si
Zitong Feng
Huiying Zhang
Hui Tian
Negatively Regulated by miR-29c-3p, MTFR1 Promotes the Progression and Glycolysis in Lung Adenocarcinoma via the AMPK/mTOR Signalling Pathway
description Background: Lung adenocarcinoma (LUAD) is the major form of lung cancer that presents a major peril to public health. Owing to the high rates of morbidity, mortality and chemoresistance, it is necessary to develop more effective therapeutic targets of LUAD. Mitochondrial fission regulator 1 (MTFR1) affects the occurrence and development of some diseases by regulating mitochondrial dynamics and is dysregulated in LUAD. However, the functions and molecular mechanisms of MTFR1 in LUAD have not been investigated.Methods: Immunohistochemical (IHC) analysis, real-time quantitative polymerase chain reaction (RT-qPCR), bioinformatic analysis and western blot (WB) were performed to assess the expression of MTFR1 at both protein and mRNA levels. The biological functions of MTFR1 in LUAD cells were assessed based on various in vivo and in vitro experiments. The dual-luciferase reporter assay and some rescue experiments were performed to evaluate the underlying mechanism of MTFR1 in LUAD.Results: MTFR1 was upregulated in LUAD cells and tissues and correlated with dismal clinicopathologic features and a worse prognosis of patients with LUAD. Functionally, MTFR1 overexpression stimulated the proliferation, invasion, migration and glycolytic capacity and impeded the apoptosis of LUAD cells; however, opposite results were obtained when MTFR1 expression was knocked down. MTFR1, which was directly targeted by miR-29c-3p, may exert its biological functions through the AMPK/mTOR signalling pathway.Conclusion: MTFR1 promotes the progression of LUAD. Therefore, targeting MTFR1 can offer an effective therapeutic strategy for LUAD treatment.
format article
author Yongmeng Li
Yanfei Liu
Kai Jin
Rui Dong
Cun Gao
Libo Si
Zitong Feng
Huiying Zhang
Hui Tian
author_facet Yongmeng Li
Yanfei Liu
Kai Jin
Rui Dong
Cun Gao
Libo Si
Zitong Feng
Huiying Zhang
Hui Tian
author_sort Yongmeng Li
title Negatively Regulated by miR-29c-3p, MTFR1 Promotes the Progression and Glycolysis in Lung Adenocarcinoma via the AMPK/mTOR Signalling Pathway
title_short Negatively Regulated by miR-29c-3p, MTFR1 Promotes the Progression and Glycolysis in Lung Adenocarcinoma via the AMPK/mTOR Signalling Pathway
title_full Negatively Regulated by miR-29c-3p, MTFR1 Promotes the Progression and Glycolysis in Lung Adenocarcinoma via the AMPK/mTOR Signalling Pathway
title_fullStr Negatively Regulated by miR-29c-3p, MTFR1 Promotes the Progression and Glycolysis in Lung Adenocarcinoma via the AMPK/mTOR Signalling Pathway
title_full_unstemmed Negatively Regulated by miR-29c-3p, MTFR1 Promotes the Progression and Glycolysis in Lung Adenocarcinoma via the AMPK/mTOR Signalling Pathway
title_sort negatively regulated by mir-29c-3p, mtfr1 promotes the progression and glycolysis in lung adenocarcinoma via the ampk/mtor signalling pathway
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/9badcc4e38704b4abec3618eded133c8
work_keys_str_mv AT yongmengli negativelyregulatedbymir29c3pmtfr1promotestheprogressionandglycolysisinlungadenocarcinomaviatheampkmtorsignallingpathway
AT yanfeiliu negativelyregulatedbymir29c3pmtfr1promotestheprogressionandglycolysisinlungadenocarcinomaviatheampkmtorsignallingpathway
AT kaijin negativelyregulatedbymir29c3pmtfr1promotestheprogressionandglycolysisinlungadenocarcinomaviatheampkmtorsignallingpathway
AT ruidong negativelyregulatedbymir29c3pmtfr1promotestheprogressionandglycolysisinlungadenocarcinomaviatheampkmtorsignallingpathway
AT cungao negativelyregulatedbymir29c3pmtfr1promotestheprogressionandglycolysisinlungadenocarcinomaviatheampkmtorsignallingpathway
AT libosi negativelyregulatedbymir29c3pmtfr1promotestheprogressionandglycolysisinlungadenocarcinomaviatheampkmtorsignallingpathway
AT zitongfeng negativelyregulatedbymir29c3pmtfr1promotestheprogressionandglycolysisinlungadenocarcinomaviatheampkmtorsignallingpathway
AT huiyingzhang negativelyregulatedbymir29c3pmtfr1promotestheprogressionandglycolysisinlungadenocarcinomaviatheampkmtorsignallingpathway
AT huitian negativelyregulatedbymir29c3pmtfr1promotestheprogressionandglycolysisinlungadenocarcinomaviatheampkmtorsignallingpathway
_version_ 1718403634435194880