Metformin suppresses NFE2L1 pathway activation to inhibit gap junction beta protein expression in NSCLC

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Autori principali: Shuo Yu, Hui Ren, Tingting Liu, Xiaoyan Han, Hui Guo, Qian Ning, Yang Li, Hong Zhou, Mingwei Chen, Tinghua Hu
Natura: Artículo Open Access
Pubblicazione: Wiley 2024
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author Shuo Yu
Hui Ren
Tingting Liu
Xiaoyan Han
Hui Guo
Qian Ning
Yang Li
Hong Zhou
Mingwei Chen
Tinghua Hu
author_facet Shuo Yu
Hui Ren
Tingting Liu
Xiaoyan Han
Hui Guo
Qian Ning
Yang Li
Hong Zhou
Mingwei Chen
Tinghua Hu
Shuo Yu
Hui Ren
Tingting Liu
Xiaoyan Han
Hui Guo
Qian Ning
Yang Li
Hong Zhou
Mingwei Chen
Tinghua Hu
collection Wiley Open Access
contents Metformin suppresses NFE2L1 pathway activation to inhibit gap junction beta protein expression in NSCLC Shuo Yu Hui Ren Tingting Liu Xiaoyan Han Hui Guo Qian Ning Yang Li Hong Zhou Mingwei Chen Tinghua Hu Cancer Medicine AbstractObjectiveNon‐small‐cell lung cancer (NSCLC) is a deadly form of cancer that exhibits extensive intercellular communication which contributed to chemoradiotherapy resistance. Recent evidence suggests that arrange of key proteins are involved in lung cancer progression, including gap junction proteins (GJPs).Methods and ResultsIn this study, we examined the expression patterns of GJPs in NSCLC, uncovering that both gap junction protein, beta 2 (GJB2) and gap junction protein, beta 2 (GJB3) are increased in LUAD and LUSC. We observed a correlation between the upregulation of GJB2, GJB3 in clinical samples and a worse prognosis in patients with NSCLC. By examining the mechanics, we additionally discovered that nuclear factor erythroid‐2‐related factor 1 (NFE2L1) had the capability to enhance the expression of connexin26 and connexin 31 in the NSCLC cell line A549. In addition, the use of metformin was discovered to cause significant downregulation of gap junction protein, betas (GJBs) by limiting the presence of NFE2L1 in the cytoplasm.ConclusionThis emphasizes the potential of targeting GJBs as a viable treatment approach for NSCLC patients receiving metformin. 10.1002/cam4.7021 http://creativecommons.org/licenses/by/4.0/
doi_str_mv 10.1002/cam4.7021
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institution Wiley Open Access
license_str_mv http://creativecommons.org/licenses/by/4.0/
publishDate 2024
publisher Wiley
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spellingShingle Metformin suppresses NFE2L1 pathway activation to inhibit gap junction beta protein expression in NSCLC
Shuo Yu
Hui Ren
Tingting Liu
Xiaoyan Han
Hui Guo
Qian Ning
Yang Li
Hong Zhou
Mingwei Chen
Tinghua Hu
Cancer Medicine
Metformin suppresses NFE2L1 pathway activation to inhibit gap junction beta protein expression in NSCLC Shuo Yu Hui Ren Tingting Liu Xiaoyan Han Hui Guo Qian Ning Yang Li Hong Zhou Mingwei Chen Tinghua Hu Cancer Medicine AbstractObjectiveNon‐small‐cell lung cancer (NSCLC) is a deadly form of cancer that exhibits extensive intercellular communication which contributed to chemoradiotherapy resistance. Recent evidence suggests that arrange of key proteins are involved in lung cancer progression, including gap junction proteins (GJPs).Methods and ResultsIn this study, we examined the expression patterns of GJPs in NSCLC, uncovering that both gap junction protein, beta 2 (GJB2) and gap junction protein, beta 2 (GJB3) are increased in LUAD and LUSC. We observed a correlation between the upregulation of GJB2, GJB3 in clinical samples and a worse prognosis in patients with NSCLC. By examining the mechanics, we additionally discovered that nuclear factor erythroid‐2‐related factor 1 (NFE2L1) had the capability to enhance the expression of connexin26 and connexin 31 in the NSCLC cell line A549. In addition, the use of metformin was discovered to cause significant downregulation of gap junction protein, betas (GJBs) by limiting the presence of NFE2L1 in the cytoplasm.ConclusionThis emphasizes the potential of targeting GJBs as a viable treatment approach for NSCLC patients receiving metformin. 10.1002/cam4.7021 http://creativecommons.org/licenses/by/4.0/
title Metformin suppresses NFE2L1 pathway activation to inhibit gap junction beta protein expression in NSCLC
topic Cancer Medicine
url https://onlinelibrary.wiley.com/doi/10.1002/cam4.7021