In-silico analysis of FASLG gene resistance in Cancer Immunotherapy

Background The FASLG gene in the TNF superfamily binds with the receptor superfamily to induce apoptosis. FAS ligand and receptor interactions lead to a dominant nature in the immune process and control cellular death (apoptosis). The dynamism of the apoptotic-induced FASLG gene controls tumour-infiltrating lymphocytes and suppresses tumour responses called tumour counter-attacks. Intense evidence in the animal model illustrated that the FASLG (CD95L) gene functions govern T-cell revival and tumour exit. The justification of CD95L (CD178) controls tumours and induces inflammation. Those mechanisms forwarded the T-cell back into the tumour context by immune checkpoints restraining tumour growth. Also, the mechanisms suggested that CD178 in tumour cells contributes to immune escape. Objective So, the study proposed an in-silico analysis of the FASLG gene and its TNF family to pursue the molecular immunologic mechanisms linked with cancer and immunity in the model organisms. Hence, the study utilized bioinformatics and computational applications to learn about the TNF domain-mediated genes in two isolated organism’s genome. This application proposed a significant way to study particular genes in the genome. Results A genome-wide observation suggested multiple hits of the TNF domains in the fundamental TNF superfamily in Homo sapiens and Mus musculus . Further observation of the FASLG gene demonstrated the nucleotides, peptides, 3D structure, domain, motifs, phylogeny, gene expression, gene network, chromosome location, and signalling pathway in humans. The study remarked that the FASLG gene and its functional mechanisms are integrated with the immune process. Concluding remarks: The documented data forward the FALSG gene and its molecular mechanisms during T-cell initiation in the tumour microenvironment. Those molecular mechanisms proposed T-cell suppression by immune checkpoints and control of tumour progression via anti-tumour immune response.