| Abstract [eng] |
Breast cancer is a multifaceted and heterogeneous disease where aberrations in genes, such as EGFR and KRAS, contribute significantly to tumor development, progression, and resistance to therapy. These genes play roles in cellular processes like proliferation, differentiation, and survival. EGFR is a receptor tyrosine kinase, and its overexpression or mutation is associated with aggressive disease and poor prognosis. Similarly, KRAS is a GTPase, and mutations in it lead to constitutive activation of downstream signaling pathways promoting oncogenesis. Therefore, understanding the impact of silencing these genes on the broader gene expression profile in different breast cancer cell lines can shed light on their roles in disease pathophysiology. This study examines the dynamic changes in gene expression in two distinct breast cancer cell lines, MCF-7 and MDA-MB-231, following exposure to gene-silencing methods targeting KRAS isoforms A and B as well as an antibody to the EGFR protein. Both cell lines represent different malignancies within breast cancer, and their molecular response to these silencing methods can provide valuable insights into the underlying mechanisms governing tumour progression and metastasis. Notably, both silencing methods had a significant impact on cellular migration potential, suggesting their influence on the metastatic capacity of these cell lines. The specific gene expression changes reflected both common and unique responses across the cell lines, underscoring the heterogeneity of breast cancer at the molecular level. These findings contribute to our understanding of the complex molecular interactions in breast cancer cells following gene silencing interventions. They provide a foundation for future investigations to further elucidate the role of KRAS and EGFR in breast cancer progression and may inform the development of more effective therapeutic strategies targeting these critical genes in different breast cancer subtypes. |
