E-Book

E-Book 3rd Congress

  • Apoptosis in Lung Cancer: A Dualistic Role and Therapeutic Implications
  • Asal Teimoori,1 Maryam Seyedolmohadesin,2,*
    1. Bachelor's student. Department of Microbiology, Faculty of Advanced Science and Technologies, Tehran Medical Science, Islamic Azad University, Tehran, Iran.
    2. Department of Genetics, Faculty of Advanced Science and Technologies, Tehran Medical Science, Islamic Azad University, Tehran, Iran.


  • Introduction: Apoptosis, a tightly controlled process of programmed cell death, plays a pivotal role in regulating tissue of growth and development, immune responses to infections and injuries, and various physiological processes. Inthe context of lung cancer, apoptosis assumes multifaceted role, exhibiting both beneficial and a detrimental aspects. When cancer cells succumb to apoptosis, it contributes to curbing tumor growth and to dissemination. However, resistance to apoptosis by cancer cells fosters their proliferation and metastasis,exacerbating the malignancy.
  • Methods: To comprehensively investigate the role of apoptosis in in Lung cancer, an extensive literature search was conducted across PubMed, Google Scholar, and NCBI databases. This search yielded 22 relevant articles that were meticulously reviewed and analyzed to gain a deeper understanding of this topic.
  • Results: Several mechanisms orchestrate the regulation of apoptosis in lung cancer. Epigenetic alterations, such as DNA methylation, can modulate gene expression, impacting apoptosis susceptibility. Notably,DNA methylation of the p76INK4a gene, which encodes a protein inhibiting cyclin-dependent kinases (CDKs),a is frequently observed in lung cancer This dysregulation of CDKs derails cell cycle regulation, potentially leading to apoptosis resistance. Mutations genes that regulate apoptosis alsos significantly influence acel'ss susceptibility to this1 process.The p53 gene stands as a crucial regulator of apoptosis. In lung cancer, mutations in p53 are commonly encountered. This gene normally functions as a tumor suppressor, preventing cells with damaged DNA from replicating However, mutated / P53 loses its regulatory capacity, allowing damagedc cells to proliferate despite their increased likelihood of malignancy. This genetic aberration fosters the development of apoptosis-resistant tumors. Furthermore, tumors can produce antiapoptotic proteins that inhibit the execution of apoptosis. One notable example is survivin, an antiapoptotic protein that blocks the activation of caspases, enzymes essential for apoptosis initiation. Excessive survivin production can prevent cancer cells from undergoing programmed cell death.
  • Conclusion: The intricate interplay of these regulatory mechanisms dictates the susceptibility of of lung cancer cells to apoptosis. Understanding these molecular pathways holds immense promise for the development of targeted and effective therapies that selectively eliminate cancer cells while preserving normal tissue functionality. By targeting these regulatory elements, we c can harness the therapeutic potential of apoptosis to combat lung cancer more effectively.
  • Keywords: Apoptosis, Lung Cancer, Epigenetics, Tumorigenesis