ArticleInternational journal of molecular sciences2024
Traversing through the Mechanistic Event Analysis in IL-6 and IL-17 Signaling for a New Therapeutic Paradigm in NSCLC.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- The dual role of the crosstalk between autophagy and ferroptosis in lung cancer treatment: Advances in mechanisms and therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- [Research Progress on Interleukin-6 in Screening and Prognosis of Patients with Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Review
- Reprogrammed MDSCs promote Th1-dominant antitumour response via CD40 induced by autocrine TNF-α after combining cryo-thermal therapy with IL6 and IL17A neutralization.Clinical and translational medicine · 2025Article
- ANCA-associated vasculitis with crescentic glomerulonephritis and papillary thyroid carcinoma: A case report.Medicine · 2025Article
- Interleukin-17A and Interleukin-17F Gene Polymorphisms in Egyptian Patients with Chronic Hepatitis C and Hepatocellular Carcinoma.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Dual signaling cascade regulating gut-lung axis in Interleukin-6/Interleukin-17 for NSCLC immuno pathogenesis.Frontiers in immunology · 2025Review
- Leveraging Evolutionary Immunology in Interleukin-6 and Interleukin-17 Signaling for Lung Cancer Therapeutics.ACS pharmacology & translational science · 2024Review
- ANCA-associated vasculitis and lung cancer: an immunological perspective.Clinical and experimental medicine · 2024Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
IL-6 and IL-17 are paradoxical cytokines that progress inflammatory states in chronic diseases, including cancer. In lung cancer, their role has been elucidated to favor cancer development by modulating signaling mechanisms critical to cellular growth. The intrinsic ability of these cytokines to influence macroautophagy is yet another reason to facilitate lung cancer. Here, we employed a systems immunology approach to discover the mechanistic role of these cytokines in cancer development. In a biological system, at later stages, the activation of NFkB stimulates immunosuppressive phenotypes to achieve tolerating effects in a transformed cell. We found that the upregulation of cytokines signaled M2 macrophages to modulate tumor responses through the activation of autophagic intermediates and inflammasome mediators. This caused immune perturbations in the tumor microenvironment, which were associated with cancer inflammation. To address these inflammatory states, we performed triggered event analysis to examine whether overexpressing immune effectors or downregulating immune suppressors may have an effect on cancer reversal. Interestingly, the inhibition of immune regulators opposed the model outcome to an increased immune response. Therefore, IL6-IL17-mediated regulation of lung cancer may address tumor malignancy and potentiate the development of newer therapeutics for NSCLC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.