FLOT1 promotes tumor development, induces epithelial–mesenchymal transition, and modulates the cell cycle by regulating the Erk/Akt signaling pathway in lung adenocarcinoma

Background FLOT1 is a scaffolding protein of lipid rafts that is believed to be involved in numerous cellular processes. However, few studies have explored the function of FLOT1 in the development of lung adenocarcinoma (LUAD) and the underlying mechanisms of FLOT1 activity. Methods FLOT1 knockdown...

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Main Authors: Louqian Zhang, Yuan Mao, Qixing Mao, Weifei Fan, Li Xu, Yan Chen, Lin Xu, Jun Wang
Format: Article
Language:English
Published: Wiley 2019-04-01
Series:Thoracic Cancer
Subjects:
Online Access:https://doi.org/10.1111/1759-7714.13027
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author Louqian Zhang
Yuan Mao
Qixing Mao
Weifei Fan
Li Xu
Yan Chen
Lin Xu
Jun Wang
author_facet Louqian Zhang
Yuan Mao
Qixing Mao
Weifei Fan
Li Xu
Yan Chen
Lin Xu
Jun Wang
author_sort Louqian Zhang
collection DOAJ
description Background FLOT1 is a scaffolding protein of lipid rafts that is believed to be involved in numerous cellular processes. However, few studies have explored the function of FLOT1 in the development of lung adenocarcinoma (LUAD) and the underlying mechanisms of FLOT1 activity. Methods FLOT1 knockdown and overexpression models were constructed via lentivirus. Cell growth, invasion, migration, and apoptosis were detected to evaluate the role of FLOT1 in LUAD development. Epithelial–mesenchymal transition (EMT) and cell cycle regulatory markers were then examined. Finally, the influence of FLOT1 on the Erk/Akt signaling pathway was investigated. Results FLOT1 promoted cell growth, invasion, and migration and inhibited cell apoptosis. In addition, FLOT1 induced EMT and modulated the cell cycle by activating the Erk/Akt signaling pathway. Conclusion The findings indicate a significant role of FLOT1 in LUAD development. Targeting FLOT1 may be a potential therapeutic strategy for LUAD.
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spelling doaj.art-4f287db7b87a4b03986ea1292f8641f92023-04-17T06:34:28ZengWileyThoracic Cancer1759-77061759-77142019-04-0110490991710.1111/1759-7714.13027FLOT1 promotes tumor development, induces epithelial–mesenchymal transition, and modulates the cell cycle by regulating the Erk/Akt signaling pathway in lung adenocarcinomaLouqian Zhang0Yuan Mao1Qixing Mao2Weifei Fan3Li Xu4Yan Chen5Lin Xu6Jun Wang7Department of Thoracic Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research Nanjing Medical University Affiliated Cancer Hospital Nanjing ChinaDepartment of Hematology and Oncology, Department of Geriatric Lung Cancer Laboratory, Geriatric Hospital of Nanjing Medical University Jiangsu Province Geriatric Hospital Nanjing ChinaDepartment of Thoracic Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research Nanjing Medical University Affiliated Cancer Hospital Nanjing ChinaDepartment of Hematology and Oncology, Department of Geriatric Lung Cancer Laboratory, Geriatric Hospital of Nanjing Medical University Jiangsu Province Geriatric Hospital Nanjing ChinaDepartment of Pathology Jiangsu Cancer Hospital Nanjing ChinaDepartment of Pathology Jiangsu Cancer Hospital Nanjing ChinaDepartment of Thoracic Surgery, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research Nanjing Medical University Affiliated Cancer Hospital Nanjing ChinaDepartment of Hematology and Oncology, Department of Geriatric Lung Cancer Laboratory, Geriatric Hospital of Nanjing Medical University Jiangsu Province Geriatric Hospital Nanjing ChinaBackground FLOT1 is a scaffolding protein of lipid rafts that is believed to be involved in numerous cellular processes. However, few studies have explored the function of FLOT1 in the development of lung adenocarcinoma (LUAD) and the underlying mechanisms of FLOT1 activity. Methods FLOT1 knockdown and overexpression models were constructed via lentivirus. Cell growth, invasion, migration, and apoptosis were detected to evaluate the role of FLOT1 in LUAD development. Epithelial–mesenchymal transition (EMT) and cell cycle regulatory markers were then examined. Finally, the influence of FLOT1 on the Erk/Akt signaling pathway was investigated. Results FLOT1 promoted cell growth, invasion, and migration and inhibited cell apoptosis. In addition, FLOT1 induced EMT and modulated the cell cycle by activating the Erk/Akt signaling pathway. Conclusion The findings indicate a significant role of FLOT1 in LUAD development. Targeting FLOT1 may be a potential therapeutic strategy for LUAD.https://doi.org/10.1111/1759-7714.13027FLOT1lung adenocarcinomamalignant behaviorsignaling pathway
spellingShingle Louqian Zhang
Yuan Mao
Qixing Mao
Weifei Fan
Li Xu
Yan Chen
Lin Xu
Jun Wang
FLOT1 promotes tumor development, induces epithelial–mesenchymal transition, and modulates the cell cycle by regulating the Erk/Akt signaling pathway in lung adenocarcinoma
Thoracic Cancer
FLOT1
lung adenocarcinoma
malignant behavior
signaling pathway
title FLOT1 promotes tumor development, induces epithelial–mesenchymal transition, and modulates the cell cycle by regulating the Erk/Akt signaling pathway in lung adenocarcinoma
title_full FLOT1 promotes tumor development, induces epithelial–mesenchymal transition, and modulates the cell cycle by regulating the Erk/Akt signaling pathway in lung adenocarcinoma
title_fullStr FLOT1 promotes tumor development, induces epithelial–mesenchymal transition, and modulates the cell cycle by regulating the Erk/Akt signaling pathway in lung adenocarcinoma
title_full_unstemmed FLOT1 promotes tumor development, induces epithelial–mesenchymal transition, and modulates the cell cycle by regulating the Erk/Akt signaling pathway in lung adenocarcinoma
title_short FLOT1 promotes tumor development, induces epithelial–mesenchymal transition, and modulates the cell cycle by regulating the Erk/Akt signaling pathway in lung adenocarcinoma
title_sort flot1 promotes tumor development induces epithelial mesenchymal transition and modulates the cell cycle by regulating the erk akt signaling pathway in lung adenocarcinoma
topic FLOT1
lung adenocarcinoma
malignant behavior
signaling pathway
url https://doi.org/10.1111/1759-7714.13027
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