Evidence map›Paper›PMID 38947555›Full record

ArticleTobacco induced diseases2024

Distinct roles and molecular mechanisms of nicotine and benzo(a)pyrene in ferroptosis of lung adenocarcinoma and lung squamous cell carcinoma.

Min G Wen, Hui X Zheng, Ying Z Zhao, Pu Xia

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Article in Tobacco induced diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

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7citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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7 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Min G WenDepartment of Community Nursing, College of Nursing, Jinzhou Medical University, Jinzhou, People's Republic of China.
Hui X ZhengTianjin Union Medical Center, Tianjin, People's Republic of China.
Ying Z ZhaoTianjin Union Medical Center, Tianjin, People's Republic of China.
Pu XiaCollege of Basic Medical Science, Jinzhou Medical University, Jinzhou, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe essence of ferroptosis is the accumulation of membrane lipid peroxides caused by increased iron, which disrupts the redox balance within cells and triggers cell death. Abnormal metabolism of iron significantly increases the risk of lung cancer and induces treatment resistance. However, the roles and mechanisms of smocking in ferroptosis in patients with lung cancer are still unclear.

methodsOur study was a secondary bioinformatics analysis followed by an experimental cell culture analysis. In this study, we identified the different ferroptosis-related genes and established the signature in lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD) patients with different smocking status, based on The Cancer Genome Atlas (TCGA) database. Fanyl diphosphate fanyl transferase 1 (FDFT1) in LUSC patients and solute carrier one family member 5 (SLC1A5) in LUAD patients were confirmed to be related to ferroptosis. Next, we checked the roles of two main components of smoke, nicotine, and benzo(a)pyrene (BaP), in ferroptosis of non-small-cell lung cancer (NSCLC) cells.

resultsWe confirmed that nicotine inhibited reactive oxygen species (ROS) levels and induced glutathione peroxidase (GPX4) expression, while the opposite roles of BaP were observed in NSCLC cells. Mechanically, nicotine protected NSCLC cells from ferroptosis through upregulation of epidermal growth factor receptor (EGFR) and SLC1A5 expression. BaP-induced ferroptosis in NSCLC cells depends on FDFT1 expression.

conclusionsIn this study, the ferroptosis-associated gene signature was identified in LUAD and LUSC patients with different smoking status. We confirmed nicotine-protected LUAD and LUSC cells from ferroptosis by upregulating EGFR and SLC1A5 expression. BaP-induced ferroptosis in these cells depends on FDFT1 expression.

Indexed as

benzo(a)pyreneferroptosisGPX4nicotinenon-small cell lung cancer

Identifiers

PMID38947555
PMCPMC11214278

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