• Examining The Receptors Involved In The Growth Of Cancer Cells And Their Effect On Cancer Treatment
  • Yasaman Peirovy,1,*
    1. Msc of Molecular Genetic Department of Genetics, Zanjan Branch, Islamic Azad University, Zanjan, Iran.


  • Introduction: The genetic and epigenetic changes that cause cancer enable cells to overproliferate and evade mechanisms that would otherwise regulate their survival and migration. Numerous of these alterations correspond to signaling pathways that regulate cell growth and division, cell death, cell fate, and cell motility. They can be understood in the context of wider signaling network distortions that fuel the progression of cancer, such as alterations in the tumor microenvironment, angiogenesis, and inflammation. Hyperactivation of these signaling pathways can result from mutations that turn cellular proto-oncogenes into oncogenes, whereas the inactivation of tumor suppressors eliminates important negative regulators of signaling. A closer look at the PI3K-Akt and Ras-ERK signaling pathways demonstrate how these changes dysregulate signaling in cancer and result in many of the defining traits of tumor cells. The aim of this study was to examine the receptors involved in the growth of cancer cells and their effect on cancer treatment.
  • Methods: The current study, which looked through academic databases like Google Scholar, Science Direct, Springer, and PubMed, Examines the receptors involved in the growth of cancer cells and their effect on cancer treatment.
  • Results: Results revealed that cancer cells exhibit a variety of distinctive traits. These are caused by cellular signal transduction dysregulation brought on by the genetic and epigenetic modifications that fuel cancer. This has an impact on not only the cancer cells themselves but also a larger signaling network that includes blood vessels, the immune system, the ECM, and other cells. In fact, systemic effects are ultimate what cause cancer patients to die because metastatic cancer is a disease that disrupts signaling throughout the affected person. Cancer therapies have been significantly impacted by pharmacological and antibody-based inhibitors that target signaling proteins downstream from these or proteins altered in malignancies. For instance, nonreceptor tyrosine kinase (NTK) Abl and receptor tyrosine kinase (RTK) ErbB2 inhibitors significantly lower patient mortality in chronic myelogenous leukemia and breast cancer, respectively. However, the incidence of recurrence is high due to the emergence of drug resistance. Other inhibitors, such as those that target B-Raf, EGFR, and the kinase ALK, generate substantial decreases in tumor volume and lengthen survival in patients with melanoma and non-small-cell lung carcinomas.
  • Conclusion: Due to the redundant pathways that regulate cell proliferation and survival, crosstalk between pathways, and feedback inhibitory mechanisms that result in pathway reactivation, the complexity of the cancer signaling network poses a significant obstacle to efforts to produce such anticancer treatments. There is the reason for optimism that methods based on targeting them will be effective because pathways like Ras-ERK and Akt-PI3K signaling regulate a wide range of characteristics of cancer cells, and because parts of these pathways, or upstream receptors, are frequently mutated in a number of cancers. However, there are a number of considerations that limit the effectiveness of medicines that target these pathways. For instance, adaptive responses to driver mutation inhibition involve rewiring of signaling pathways, and this is frequently the result of either the loss of feedback inhibition or the stimulation of stress pathways. Furthermore, despite the targeted pathways' blockage, elements from the tumor microenvironment may promote other pathways that keep cells viable. As an alternative, drug-resistant variants of the targeted protein or mutations in other pathways that get around the dependence on the targeted pathway may be selected for in some rare tumor cells, and epigenetic or stochastic changes in the state of tumor cells can also activate intrinsic resistance pathways.
  • Keywords: receptors, cancer cells, drug-resistant, epigenetic