By coupling our knowledge of signaling pathways via systems biology with efficient experimental tools, optimum therapeutics may be possible for each individual. cause of cancer death, lung cancer claims 1.3 million lives worldwide every year[1], 160000 of which come from the United States alone[2]. Lung cancer causes more deaths than colon, breast, and prostate cancers combined, accounting for 28% of all cancer deaths[3]. Over half Sipatrigine of patients with lung cancer die within one year of diagnosis[4]. While lung cancer can be caused by a variety of genetic and environmental influences, tobacco smoking contributes to 80% to 90% of lung cancer deaths, followed by radon exposure, second-hand smoking, and occupational exposure[5]. There are two major types of primary lung cancer: non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). Because these two lung cancer types differ histopathologically, they grow and proliferate differently. Histologically, NSCLC is a heterogeneous aggregate that includes squamous cell carcinoma, large cell carcinoma, and adenocarcinoma[6]. SCLC is distinguished from NSCLC by its rapid doubling time, high growth fraction, and early development of widespread metastases[7]. NSCLC accounts for 80% of clinical lung cancer cases, the remaining lung cancer cases are diagnosed as SCLC. Although both NSCLC and SCLC may be caused by tobacco smoking, SCLC is found to occur almost exclusively in smokers[8], with 90% of the patients being smokers or former smokers. Regardless of the cause, variations in the biological behaviors of these two lung cancer cell types impose challenges to their accurate prognosis and medical treatment. Conventional first-line treatments for lung cancer include surgical resection, chemotherapy, Sipatrigine and radiation[9]. Although the former may be suggested to patients during the early stages of NSCLC, the highly proliferative and metastatic nature of SCLC deems operation almost futile because microscopic cells separated from the primary mass may still remain in the body despite surgical resection. However, chemotherapy and radiotherapy serve as cornerstone treatments for SCLC and advanced NSCLC, offering modest survival benefits at the expense of severe and unpleasant side effects[10], despite having improved median survival rates and recurrence when used in combination[11]. As the standard therapy for NSCLC, platinum-based chemotherapy regimens are relatively effective due to their ability to cause DNA crosslinks that inhibit DNA repair or synthesis in cancer cells[12]. However, these regimens have limitations. Their association with severe toxicities, in addition to the multiple drug-resistant nature of NSCLC cells, reduce the efficacy of the treatment[13]. As conventional treatments for NSCLC patients reach a therapeutic plateau, research efforts Rabbit Polyclonal to RAB41 have been made to discover novel agents that target lung cancer-related oncogenes for the optimum treatment. Targeted cancer therapies focus on blocking the growth and spreading of cancer by interfering with specific molecules involved in tumor growth and progression. Research endeavors in targeted cancer therapy have focused on studying proteins that govern basic cellular functions that interfere with cell growth signaling, tumor blood vessel development, selective apoptosis, immunity stimulation, and drug delivery to specific target sites. With the advance of experimental techniques, systems biology has become an emerging approach to map the complex interactions within biological systems that may broaden our understanding of metabolic and cell signaling networks[6]. Coupled with bioinformatics and Proteomics, protein-protein Sipatrigine interaction (PPI) analyses enable the identification and discovery of previously unknown protein functions. Not only does PPI network facilitate our understanding of the molecular mechanisms underlying lung cancer, it may serve as an important tool for identifying diagnostic molecular markers to predict patient susceptibility and detect early stages of lung cancer. PPI network allows several molecular targets to be identified. Ray gene[24]. In heavy smokers, Oncogene mutations are the dominant promoter of the activation of oncogenic.