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)...
Guardado en:
Autores principales: | , , , , , , , , |
---|---|
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 |