Deciphering the Molecular Dynamics of Liver Cancer: Insights into Pathogenesis and Therapeutic Opportunities

سال انتشار: 1403
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 97

نسخه کامل این مقاله ارائه نشده است و در دسترس نمی باشد

استخراج به نرم افزارهای پژوهشی:

لینک ثابت به این مقاله:

شناسه ملی سند علمی:

ICGCS02_107

تاریخ نمایه سازی: 17 دی 1403

چکیده مقاله:

Hepatocellular carcinoma, a type of cancer, is one of the most challenging malignancies to cure due to its complex molecular underpinning. Any attempt to establish effective treatments needs a good understanding of the complicated molecular interactions that drive the initiation and progression of tumors, as well as their response to therapy. This review epitomizes an overview of the complexity with which genetic alterations, signaling pathways, and microenvironmental factors in liver cancer may befall that contribute to its pathogenesis. Method This review discusses the genetic mutations propelling this disease and the dysregulation of signaling pathways, epigenetic alterations, and the tumor microenvironment. We also analyze critical oncogenes and tumor suppressor genes and the impact of their aberrant pathways on tumor behavior. In addition, we cover the latest research on how cells communicate with each other at the tumor microenvironment level, such as the role of exosomes in intercellular communication and how this communication influences tumor advancement and response to treatments. Results Our study has pointed out some key findings of the hepatocarcinoma molecular landscape: - Genetic Alterations: Mutations in oncogenes like CTNNB۱ (β-catenin), TP۵۳, and TERT, as well as changes in tumor suppressor genes like PTEN and AXIN۱, disrupt critical cellular processes. These alterations result in uncontrolled cell proliferation and resistance to programmed cell death. - Dysregulated Pathways: There is frequent activation of specific key pathways in HCC, which include Wnt/β-catenin and PI۳K/Akt/mTOR. The atypical activation of the Wnt/β-catenin pathway results in aberrant cellular proliferation, while shifts in the TGF-β signaling pathway result in immune escape. All these events contribute to the aggressiveness of liver tumors. - Epigenetic features: Aberrant DNA methylation and histone modifications affect gene expression levels regarding the cell cycle and apoptosis. Additionally, these epigenetic changes in tumor cells affect the immune landscape in the tumor microenvironment. - Tumor Microenvironment: The stroma surrounding the tumor plays a significant role in developing liver cancer. Tumor-associated stromal cells produce cytokines and growth factors that aid angiogenesis and metastasis. The immune-suppressive environment also inhibits effective immune responses to cancerous tumors. Conclusion Deciphering the molecular dynamics of liver cancer will help us comprehend its pathogenesis and potential treatment approaches. The better elucidation of how genetic mutations and the dysregulation of signaling pathways communicate with microenvironmental factors underlines critical vulnerabilities in HCC and ushers new and promising avenues for targeted therapies. Nevertheless, due to the complexity of liver cancer biology, the systems for developing a far-reaching strategy in fighting such a resistant disease will not be created without a multidisciplinary approach integrating molecular biology, oncology, and immunology.

نویسندگان

Sana Tarashandeh Hemmati

Undergraduate Student of Cellular and Molecular Biology - Genetics, Faculty of Basic Sciences, Islamic Azad University, Lahijan Branch

Ali Salehzadeh

Associate Professor, Department of Biology, Azad University, Rasht Branch