Cellular Senescence in Lung Cancer: Molecular Mechanisms and Therapeutic Interventions.

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dc.contributor.authorJha, S.K.
dc.contributor.authorDe Rubis, G.
dc.contributor.authorDevkota, S.R.
dc.contributor.authorZhang, Y.
dc.contributor.authorAdhikari, R.
dc.contributor.authorJha, L.A.
dc.contributor.authorBhattacharya, K.
dc.contributor.authorMehndiratta, S.
dc.contributor.authorGupta, G.
dc.contributor.authorSingh, S.K.
dc.contributor.authorPanth, N.
dc.contributor.authorDua, K.
dc.contributor.authorHansbro, P.M.
dc.contributor.authorPaudel, K.R.
dc.date.issued2024
dc.description.abstractLung cancer stands as the primary contributor to cancer-related fatalities worldwide, affecting both genders. Two primary types exist where non-small cell lung cancer (NSCLC), accounts for 80–85% and SCLC accounts for 10–15% of cases. NSCLC subtypes include adenocarcinoma, squamous cell carcinoma, and large cell carcinoma. Smoking, second-hand smoke, radon gas, asbestos, and other pollutants, genetic predisposition, and COPD are lung cancer risk factors. On the other hand, stresses such as DNA damage, telomere shortening, and oncogene activation cause a prolonged cell cycle halt, known as senescence. Despite its initial role as a tumor-suppressing mechanism that slows cell growth, excessive or improper control of this process can cause age-related diseases, including cancer. Cellular senescence has two purposes in lung cancer. Researchers report that senescence slows tumor growth by constraining multiplication of impaired cells. However, senescent cells also demonstrate the pro-inflammatory senescence-associated secretory phenotype (SASP), which is widely reported to promote cancer. This review will look at the role of cellular senescence in lung cancer, describe its diagnostic markers, ask about current treatments to control it, look at case studies and clinical trials that show how senescence-targeting therapies can be used in lung cancer, and talk about problems currently being faced, and possible solutions for the same in the future.
dc.description.statementofresponsibilitySaurav Kumar Jha, Gabriele De Rubis, Shankar Raj Devkota, Yali Zhang, Radhika Adhikari, Laxmi Akhileshwar Jha, Kunal Bhattacharya, Samir Mehndiratta, Gaurav Gupta, Sachin Kumar Singh, Nisha Panth, Kamal Dua, Philip M. Hansbro, Keshav Raj Paudel
dc.identifier.citationAgeing Research Reviews, 2024; 97:102315-1-102315-21
dc.identifier.doi10.1016/j.arr.2024.102315
dc.identifier.issn1568-1637
dc.identifier.issn1872-9649
dc.identifier.orcidDevkota, S.R. [0000-0002-3154-7928]
dc.identifier.orcidZhang, Y. [0000-0003-0107-4274]
dc.identifier.urihttps://hdl.handle.net/2440/146634
dc.language.isoen
dc.publisherElsevier
dc.rights© 2024 The Author(s). Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
dc.source.urihttps://doi.org/10.1016/j.arr.2024.102315
dc.subjectcellular senescence; Tumor; Lung cancer; Senescence-associated secretory phenotype; Senescence-targeting therapies
dc.subject.meshAnimals
dc.subject.meshHumans
dc.subject.meshCarcinoma, Non-Small-Cell Lung
dc.subject.meshLung Neoplasms
dc.subject.meshCellular Senescence
dc.titleCellular Senescence in Lung Cancer: Molecular Mechanisms and Therapeutic Interventions.
dc.typeJournal article
pubs.publication-statusPublished

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