دورية أكاديمية
Particulate matters 2.5 induce tumor progression in lung cancer by increasing the activity of hnRNPA2B1 resulting in retarding mRNA decay of oxidative phosphorylation.
العنوان: | Particulate matters 2.5 induce tumor progression in lung cancer by increasing the activity of hnRNPA2B1 resulting in retarding mRNA decay of oxidative phosphorylation. |
---|---|
المؤلفون: | Bian W; Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China., Yu H; Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China., Zhang X; Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China., Wang Y; Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China., Ni B; Department of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China. |
المصدر: | IUBMB life [IUBMB Life] 2024 Aug; Vol. 76 (8), pp. 563-576. Date of Electronic Publication: 2024 Mar 07. |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: Published for the International Union of Biochemistry and Molecular Biology by Taylor & Francis Country of Publication: England NLM ID: 100888706 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1521-6551 (Electronic) Linking ISSN: 15216543 NLM ISO Abbreviation: IUBMB Life Subsets: MEDLINE |
أسماء مطبوعة: | Original Publication: London ; Philadelphia, PA : Published for the International Union of Biochemistry and Molecular Biology by Taylor & Francis, c1999- |
مواضيع طبية MeSH: | Apoptosis* , Heterogeneous-Nuclear Ribonucleoprotein Group A-B*/metabolism , Heterogeneous-Nuclear Ribonucleoprotein Group A-B*/genetics , Lung Neoplasms*/pathology , Lung Neoplasms*/genetics , Lung Neoplasms*/metabolism , Oxidative Phosphorylation* , Particulate Matter*/adverse effects , RNA Stability*, Animals ; Humans ; Mice ; A549 Cells ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Mice, Inbred BALB C ; Mice, Nude ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Xenograft Model Antitumor Assays |
مستخلص: | Particulate matter 2.5 (PM2.5) has been implicated in lung injury and various cancers, yet its precise mechanistic role remains elusive. To elucidate the key signaling pathways underpinning PM2.5-induced lung cancer progression, we embarked on a study examining the impact of PM2.5 both in vitro and in vivo. Lung cancer cell lines, A549 and H157, were employed for the in vitro investigations. Overexpression or knockdown techniques targeting the hnRNPA2B1 protein were implemented. Lung cancer cells were treated with a medium containing PM2.5 and subsequently prepared for in vitro evaluations. Cell growth, invasion, and migration were gauged using transwell and CCK-8 assays. Apoptosis was ascertained through flow cytometry and western blotting of pertinent proteins. Seahorse analyses probed the influence of PM2.5 on lung cancer energy metabolism. The RNA stability assay was employed to discern the impact of PM2.5 on the stability of oxidative phosphorylation-related genes in lung cancer. Our findings revealed that PM2.5 augmented cell proliferation, migration, and invasion rates. Similarly, a diminished apoptosis rate was observed in PM2.5-treated cells. Elevated expression of hnRNPA2B1 was detected in lung cancer cells exposed to PM2.5. Moreover, in cells treated with PM2.5, hnRNPA2B1 knockdown markedly curtailed cell proliferation by inducing G1-S cell cycle arrest and bolstered lung cancer cell apoptosis in vitro; it also curbed xenograft tumor growth. Mechanistically, our data suggest that PM2.5 undermines the stability of mRNA transcripts associated with oxidative phosphorylation (OXPHOS) and augments the formation of processing bodies (P-bodies), leading to an upsurge in OXPHOS levels. In conclusion, PM2.5 appears to drive lung cancer progression and migration by modulating the energy metabolism of lung cancer in a hnRNPA2B1-dependent manner. (© 2024 International Union of Biochemistry and Molecular Biology.) |
References: | Badyda AJ, Grellier J, Dąbrowiecki P. Ambient PM2. 5 exposure and mortality due to lung cancer and cardiopulmonary diseases in Polish cities. Respiratory Treatment and Prevention. Berlin: Springer; 2016. p. 9–17. De Marco A, Amoatey P, Khaniabadi YO, Sicard P, Hopke PK. Mortality and morbidity for cardiopulmonary diseases attributed to PM2. 5 exposure in the metropolis of Rome, Italy. Eur J Intern Med. 2018;57:49–57. Billet S, Garçon G, Dagher Z, Verdin A, Ledoux F, Cazier F, et al. Ambient particulate matter (PM2. 5): physicochemical characterization and metabolic activation of the organic fraction in human lung epithelial cells (A549). Environ Res. 2007;105:212–223. Wang N, Mengersen K, Tong S, Kimlin M, Zhou M, Wang L, et al. Short‐term association between ambient air pollution and lung cancer mortality. Environ Res. 2019;179:108748. Yang X, Zhang T, Zhang X, Chu C, Sang S. Global burden of lung cancer attributable to ambient fine particulate matter pollution in 204 countries and territories, 1990–2019. Environ Res. 2022;204:112023. Bai L, Shin S, Burnett RT, Kwong JC, Hystad P, van Donkelaar A, et al. Exposure to ambient air pollution and the incidence of lung cancer and breast cancer in the Ontario Population Health and Environment Cohort. Int J Cancer. 2020;146:2450–2459. Crouse DL, Peters PA, Hystad P, Brook JR, van Donkelaar A, Martin RV, et al. Ambient PM2. 5, O3, and NO2 exposures and associations with mortality over 16 years of follow‐up in the Canadian Census Health and Environment Cohort (CanCHEC). Environ Health Perspect. 2015;123:1180–1186. Nagel G, Stafoggia M, Pedersen M, Andersen ZJ, Galassi C, Munkenast J, et al. Air pollution and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Int J Cancer. 2018;143:1632–1643. Su S‐Y, Liaw Y‐P, Jhuang J‐R, Hsu S‐Y, Chiang C‐J, Yang Y‐W, et al. Associations between ambient air pollution and cancer incidence in Taiwan: an ecological study of geographical variations. BMC Public Health. 2019;19:1–8. Thangavel P, Park D, Lee Y‐C. Recent insights into particulate matter (PM2. 5)‐mediated toxicity in humans: an overview. Int J Environ Res Public Health. 2022;19:7511. Turner MC, Krewski D, Pope CA III, Chen Y, Gapstur SM, Thun MJ. Long‐term ambient fine particulate matter air pollution and lung cancer in a large cohort of never‐smokers. Am J Respir Crit Care Med. 2011;184:1374–1381. Al‐Khafaji AS, Marcus MW, Davies M, Risk JM, Shaw RJ, Field JK, et al. hnRNPA2B1 mRNA expression is an independent predictor of poor prognosis in patients with non‐small cell lung cancer. Oncol Lett. 2017;13:4463–4468. Jungwirth G, Yu T, Cao J, Eddine MA, Moustafa M, Warta R, et al. KIF11 inhibitors filanesib and ispinesib inhibit meningioma growth in vitro and in vivo. Cancer Lett. 2021;506:1–10. Zhang M‐Y, Liu X‐X, Li H, Li R, Liu X, Qu Y‐Q. Elevated mRNA levels of hnRNPA2B1, CDC20 and TPX2 are associated with poor prognosis of smoking related lung adenocarcinoma using bioinformatics analysis. Int J Med Sci. 2018;15:1676–1685. Linardopoulos S. Aurora‐a kinase regulates NF‐kappaB activity: lessons from combination studies. J BUON. 2007;12:S67–S70. Orth M, Unger K, Schoetz U, Belka C, Lauber K. Taxane‐mediated radiosensitization derives from chromosomal missegregation on tripolar mitotic spindles orchestrated by hnRNPA2B1 and TPX2. Oncogene. 2018;37:52–62. Shah KN, Bhatt R, Rotow J, Rohrberg J, Olivas V, Wang VE, et al. Aurora kinase A drives the evolution of resistance to third‐generation EGFR inhibitors in lung cancer. Nat Med. 2019;25:111–118. Sun C, Chan F, Briassouli P, Linardopoulos S. Aurora kinase inhibition downregulates NF‐κB and sensitises tumour cells to chemotherapeutic agents. Biochem Biophys Res Commun. 2007;352:220–225. Min YH, Kim W, Kim J‐E. The Aurora kinase A inhibitor TC‐A2317 disrupts mitotic progression and inhibits cancer cell proliferation. Oncotarget. 2016;7:84718–84735. Tan J, Xu W, Lei L, Liu H, Wang H, Cao X, et al. Inhibition of aurora kinase a by alisertib reduces cell proliferation and induces apoptosis and autophagy in huh‐6 human hepatoblastoma cells. Onco Targets Ther. 2020;13:3953–3963. Chang C‐H, Bijian K, Wernic D, Su J, da Silva SD, Yu H, et al. A novel orally available seleno‐purine molecule suppresses triple‐negative breast cancer cell proliferation and progression to metastasis by inducing cytostatic autophagy. Autophagy. 2019;15:1376–1390. Damodaran AP, Vaufrey L, Gavard O, Prigent C. Aurora a kinase is a priority pharmaceutical target for the treatment of cancers. Trends Pharmacol Sci. 2017;38:687–700. Kafasla P, Skliris A, Kontoyiannis DL. Post‐transcriptional coordination of immunological responses by RNA‐binding proteins. Nat Immunol. 2014;15:492–502. Houseley J, Tollervey D. The many pathways of RNA degradation. Cell. 2009;136:763–776. Chen C‐YA, Shyu A‐B. Deadenylation and P‐bodies. Ten Years of Progress in GW/P Body Research. New York: Springer; 2013. p. 183–195. Anderson P, Kedersha N, Ivanov P. Stress granules, P‐bodies and cancer. Biochimica et Biophysica Acta (BBA)‐Gene Regulatory Mechanisms. 2015;1849:861–870. Yang B, Chen D, Zhao H, Xiao C. The effects for PM2. 5 exposure on non‐small‐cell lung cancer induced motility and proliferation. Springerplus. 2016;5:1–9. Wang G‐Z, Cheng X, Zhou B, Wen Z‐S, Huang Y‐C, Chen H‐B, et al. The chemokine CXCL13 in lung cancers associated with environmental polycyclic aromatic hydrocarbons pollution. Elife. 2015;4:e09419. Gao S‐H, Liu S‐Z, Wang G‐Z, Zhou G‐B. CXCL13 in cancer and other diseases: biological functions, clinical significance, and therapeutic opportunities. Life. 2021;11:1282. Niu L, Gao C, Li Y. Identification of potential core genes in colorectal carcinoma and key genes in colorectal cancer liver metastasis using bioinformatics analysis. Sci Rep. 2021;11:1–14. Wang H, Li S, Wang Q, Jin Z, Shao W, Gao Y, et al. Tumor immunological phenotype signature‐based high‐throughput screening for the discovery of combination immunotherapy compounds. Sci Adv. 2021;7:eabd7851. |
فهرسة مساهمة: | Keywords: RNPA2B1; energy metabolism; lung cancer; oxidative phosphorylation; particulate matter |
المشرفين على المادة: | 0 (Heterogeneous-Nuclear Ribonucleoprotein Group A-B) 0 (hnRNP A2) 0 (Particulate Matter) 0 (RNA, Messenger) |
تواريخ الأحداث: | Date Created: 20240307 Date Completed: 20240731 Latest Revision: 20240814 |
رمز التحديث: | 20240814 |
DOI: | 10.1002/iub.2813 |
PMID: | 38450584 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1521-6551 |
---|---|
DOI: | 10.1002/iub.2813 |