With a 5-year survival rate of only 15%, non-small cell lung cancer (NSCLC), the most common kind of lung carcinoma and the cause of millions of deaths annually, has drawn attention. Numerous variables, such as disrupted signaling caused by somatic mutations in the EGFR-mediated RAS/RAF/MAPK, PI3K/AKT, JAK/STAT signaling cascade, supports tumour survival in one way or another. Here, the tumour microenvironment significantly contributes to the development of cancer by thwarting the immune response. MicroRNAs (miRNAs) are critical regulators of gene expression that can function as oncogenes or oncosuppressors. They have a major influence on the occurrence and prognosis of NSCLC. Though, a myriad number of therapies are available and many are being clinically tested, still the drug resistance, its adverse effect and toxicity leading towards fatality cannot be ruled out. In this review, we tried to ascertain the missing links in between perturbed EGFR signaling, miRNAs favouring tumorigenesis and the autophagy mechanism. While connecting all the aforementioned points multiple associations were set, which can be targeted in order to combat NSCLC. Here, we tried illuminating designing synthetically engineered circuits with the toggle switches that might lay a prototype for better therapeutic paradigm.

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Increasing research suggests that sphingolipid metabolism is essential for the progression and metastasis of cancer. The underlying mechanistic insight into the dysregulation of sphingolipid metabolism affecting pathways is poorly investigated. As a result, the goal of the current study was to glean knowledge from the systems biology approach to investigate how the sphingolipid metabolism affects the signal transduction network in non‐small cell lung cancer (NSCLC), the most common type of cancer in terms of occurrence and death globally. Our paper includes system‐level models representing the diseased and healthy states elucidating that sphingolipids and its enzymes mediate PI3K/AKT pathway. Notably, its activation of downstream signaling mediators has led to cancer growth. Considering the critical role of sphingolipids in NSCLC, our study advocates the target CERS6 which can be potentially inhibited using hsa‐miR‐520c‐3p to combat NSCLC for future precision medicine.