Investigating regulated signaling pathways in therapeutic targeting of non-small cell lung carcinoma
Non-small cell lung carcinoma (NSCLC) is the most common malignancy worldwide. The signaling cascades are stimulated via genetic modifications in upstream signaling molecules, which affect apoptotic, proliferative, and differentiation pathways. Dysregulation of these signaling cascades causes cancer...
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Veröffentlicht in: | Biomedicine & pharmacotherapy 2023-05, Vol.161, p.114452-114452, Article 114452 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Non-small cell lung carcinoma (NSCLC) is the most common malignancy worldwide. The signaling cascades are stimulated via genetic modifications in upstream signaling molecules, which affect apoptotic, proliferative, and differentiation pathways. Dysregulation of these signaling cascades causes cancer-initiating cell proliferation, cancer development, and drug resistance. Numerous efforts in the treatment of NSCLC have been undertaken in the past few decades, enhancing our understanding of the mechanisms of cancer development and moving forward to develop effective therapeutic approaches. Modifications of transcription factors and connected pathways are utilized to develop new treatment options for NSCLC. Developing designed inhibitors targeting specific cellular signaling pathways in tumor progression has been recommended for the therapeutic management of NSCLC. This comprehensive review provided deeper mechanistic insights into the molecular mechanism of action of various signaling molecules and their targeting in the clinical management of NSCLC.
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•Dysregulation of signaling cascades induces cell proliferation, and drug resistance in NSCLC.•This review provides deeper mechanistic insights into different signaling pathways in NSCLC development.•Roles of important signaling cascades in NSCLC and their subsequent therapeutic implications are discussed.•We further described how the targeting of these pathways could be helpful to prevent NSCLC. |
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ISSN: | 0753-3322 1950-6007 |
DOI: | 10.1016/j.biopha.2023.114452 |