Chronic inflammation has emerged as a key player at different stages of cancer development. A prominent signaling pathway for acute and chronic inflammation is the activation of the caspase-1 inflammasomes. These are complexes that assemble on activation of certain nucleotide-binding domain, leucine-rich repeat containing proteins (NLRs), AIM2-like receptors (ALRs), or pyrin due to activation via PAMPs or DAMPs. Of these, five complexes-NLRP1, NLRP3, NLRC4, Pyrin, and AIM2 are of importance in the context of cancer for their activities in modulating immune responses, cell proliferation, and apoptosis. Inflammasomes have emerged as clinically relevant in multiple forms of cancer making them highly promising targets for cancer therapy. As lungs are a tissue niche that is prone to inflammation owing to its exposure to external substances, inflammasomes play a vital role in the development and pathogenesis of lung cancer. Therefore, manipulation of inflammasome by various immunomodulatory means could prove a full-proof strategy for the treatment of lung cancer. Here, in this review, we tried to explore the various strategies to target the inflammasomes for the treatment of lung cancer.
Keyphrases
- oxidative stress
- papillary thyroid
- signaling pathway
- cell proliferation
- cancer therapy
- immune response
- squamous cell
- pi k akt
- drug delivery
- lymph node metastasis
- squamous cell carcinoma
- endoplasmic reticulum stress
- liver failure
- cell cycle
- induced apoptosis
- drug induced
- epithelial mesenchymal transition
- childhood cancer
- drinking water
- inflammatory response
- combination therapy
- cell cycle arrest
- dendritic cells
- intensive care unit
- respiratory failure
- extracorporeal membrane oxygenation
- nlrp inflammasome
- hepatitis b virus
- replacement therapy
- dna binding