Endogenous IL-33 inhibits apoptosis in non-small cell lung cancer cells by regulating BCL2/BAX via the ERK1/2 pathway

Abstract Lung cancer remains a leading cause of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) accounting for 85% of cases. Although targeted therapies have improved treatment outcomes, drug resistance poses a significant challenge, underscoring the need for novel therap...

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Main Authors: Liping Liu, Haoge Luo, Yingdong Xie, Ying Wang, Shiying Ren, Haiyang Sun, Zhuoyuan Xin, Dong Li
Format: Article
Language:English
Published: Nature Portfolio 2025-02-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-91202-w
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author Liping Liu
Haoge Luo
Yingdong Xie
Ying Wang
Shiying Ren
Haiyang Sun
Zhuoyuan Xin
Dong Li
author_facet Liping Liu
Haoge Luo
Yingdong Xie
Ying Wang
Shiying Ren
Haiyang Sun
Zhuoyuan Xin
Dong Li
author_sort Liping Liu
collection DOAJ
description Abstract Lung cancer remains a leading cause of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) accounting for 85% of cases. Although targeted therapies have improved treatment outcomes, drug resistance poses a significant challenge, underscoring the need for novel therapeutic strategies. Interleukin-33 (IL-33), a member of the IL-1 superfamily, functions both as a nuclear protein and a cytokine, binding to its receptor, ST2. While IL-33 is known to promote tumour cell migration and metastasis, its role in regulating apoptosis remains incompletely understood. In this study, we focused on endogenous IL-33, employing lentiviral transfection to overexpress both the full-length and mature forms of IL-33 in lung cancer cells. We examined its effects on apoptosis in vitro and investigated the underlying molecular mechanisms. Our findings reveal that endogenous IL-33 inhibits apoptosis in lung cancer cells by modulating the expression of BCL2 and BAX via the ERK1/2 pathway in an autocrine manner. These results uncover a novel mechanism of IL-33-mediated tumour survival and provide a foundation for the development of IL-33/ST2-targeted therapies in NSCLC.
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issn 2045-2322
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spelling doaj-art-05b33dfdf5144c1a944d01e830e244332025-08-20T03:11:07ZengNature PortfolioScientific Reports2045-23222025-02-0115111210.1038/s41598-025-91202-wEndogenous IL-33 inhibits apoptosis in non-small cell lung cancer cells by regulating BCL2/BAX via the ERK1/2 pathwayLiping Liu0Haoge Luo1Yingdong Xie2Ying Wang3Shiying Ren4Haiyang Sun5Zhuoyuan Xin6Dong Li7Key Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin UniversityKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin UniversityKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin UniversityKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin UniversityKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin UniversityKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin UniversityKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin UniversityKey Laboratory of Pathobiology, Ministry of Education, College of Basic Medical Sciences, Jilin UniversityAbstract Lung cancer remains a leading cause of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) accounting for 85% of cases. Although targeted therapies have improved treatment outcomes, drug resistance poses a significant challenge, underscoring the need for novel therapeutic strategies. Interleukin-33 (IL-33), a member of the IL-1 superfamily, functions both as a nuclear protein and a cytokine, binding to its receptor, ST2. While IL-33 is known to promote tumour cell migration and metastasis, its role in regulating apoptosis remains incompletely understood. In this study, we focused on endogenous IL-33, employing lentiviral transfection to overexpress both the full-length and mature forms of IL-33 in lung cancer cells. We examined its effects on apoptosis in vitro and investigated the underlying molecular mechanisms. Our findings reveal that endogenous IL-33 inhibits apoptosis in lung cancer cells by modulating the expression of BCL2 and BAX via the ERK1/2 pathway in an autocrine manner. These results uncover a novel mechanism of IL-33-mediated tumour survival and provide a foundation for the development of IL-33/ST2-targeted therapies in NSCLC.https://doi.org/10.1038/s41598-025-91202-wIL-33ST2Non-small-cell lung cancerApoptosis
spellingShingle Liping Liu
Haoge Luo
Yingdong Xie
Ying Wang
Shiying Ren
Haiyang Sun
Zhuoyuan Xin
Dong Li
Endogenous IL-33 inhibits apoptosis in non-small cell lung cancer cells by regulating BCL2/BAX via the ERK1/2 pathway
Scientific Reports
IL-33
ST2
Non-small-cell lung cancer
Apoptosis
title Endogenous IL-33 inhibits apoptosis in non-small cell lung cancer cells by regulating BCL2/BAX via the ERK1/2 pathway
title_full Endogenous IL-33 inhibits apoptosis in non-small cell lung cancer cells by regulating BCL2/BAX via the ERK1/2 pathway
title_fullStr Endogenous IL-33 inhibits apoptosis in non-small cell lung cancer cells by regulating BCL2/BAX via the ERK1/2 pathway
title_full_unstemmed Endogenous IL-33 inhibits apoptosis in non-small cell lung cancer cells by regulating BCL2/BAX via the ERK1/2 pathway
title_short Endogenous IL-33 inhibits apoptosis in non-small cell lung cancer cells by regulating BCL2/BAX via the ERK1/2 pathway
title_sort endogenous il 33 inhibits apoptosis in non small cell lung cancer cells by regulating bcl2 bax via the erk1 2 pathway
topic IL-33
ST2
Non-small-cell lung cancer
Apoptosis
url https://doi.org/10.1038/s41598-025-91202-w
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