Lung carcinoma stands as a tough challenge in the fight against cancer. The high mortality rate reflects its aggressive biological behavior, driven by genetic mutations and alterations in key oncogenes and tumor suppressor genes. The Early Growth Response-1 (EGR1) is a key regulatory factor implicated in cancer progression by undertaking a comparative characterization and identification of pathway-specific differences in EGR1 expression, understanding the significance in cancer biology. It is located in the chromosomal region of human 5q23-31. It consists of 543 amino acids and three Cys2-His2 DNA binding domains: activation domain, repressor domain, nuclear localization domain, and weak activation domain. However, the transcription of EGR1 depends on the RAS-RAF-MEK1/2-ERK1/2 signal transduction pathway, a key component of the mitogen-activated protein kinase (MAPK) cascade. This pathway facilitates the activation of EGR1 in response to extracellular signals such as growth factors, cytokines, and stress stimuli. Once activated, EGR1 functions as a transcription factor, modulating the expression of its downstream target genes, which are yet to be explored in the proposed work. Depending on the cellular context, EGR1 can either promote or suppress the transcription of genes involved in various oncogenic processes. The EGR1 interacts with critical tumor suppressors like P53, regulating apoptosis and cell cycle checkpoints and influencing oncogenic signaling pathways. Notably, among the most variable genes, EGR1 is the downstream effector of the MAPK signaling pathway, which performs the regulatory function in cell proliferation, tumor invasion, and immune regulation (Pavithran et al., 2023). Our hypothesis is to determine how CGs modulate translational processes, ultimately influencing protein expression upon treatment. How can the EGR1 be activated through the MAPK pathway by different growth factors? Will the EGR1 act on the promoter of p53-inducing expression, further activating and forming a feedback loop? We aim to elucidate the molecular mechanisms through which CGs impact signaling cascades, leading to alterations in EGR1 activity, which further elucidates its anticancer role in human lung cancer. The novelty of the proposed project lies in exploring the potent anticancer properties of CGs by their influential role over transcription, translation, and expressional differences on signaling cascades, shedding light on potential target genes, and elucidating the molecular mechanism of action in human lung Carcinoma.