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Loss of BCL6 transcriptional repressor impacts migration but not viability in MCF-7 breast cancer cells
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Orientador(es)
Resumo(s)
Breast cancer (BC) incidence has risen over the past two decades, now being the most prevalent cancer worldwide and the second leading cause of cancer-related deaths. Despite advancements in BC treatment, challenges like acquired resistance, recurrence, and metastasis persist. BCL6, a transcriptional repressor, acts as an oncogene in BC, being downregulated in about half of primary tumors of all BC subtypes and associated with disease progression and poor patient prognosis. This underscores the need to better understand BCL6 role in BC development.
Therefore, we used RNA interference to explore the impact of BCL6 depletion on the oncogenic progression of MCF-7 cells, a low-tumorigenic estrogen receptor-positive cell line. While BCL6 is known to regulate normal mammary cell proliferation and differentiation, its depletion did not affect MCF-7 cell proliferation or viability but significantly reduced their individual and collective migratory properties. RNA microarray analysis identified a set of genes upregulated following BCL6 depletion, including S100A7, previously reported to inhibit MCF-7 cell migration and invasion by reducing MMP9 secretion. However, our findings showed that S100A7 downregulation alone did not affect MCF-7 migration. Moreover, simultaneous depletion of BCL6 and S100A7 failed to restore MCF-7 cell migratory behavior.
Descrição
Abstract disponível em: Molecular Oncology. Abstracts. Mol Oncol. 2025;19:1–940. doi:10.1002/1878-0261.70070
Palavras-chave
Cancer Cells Breast Cancer (BC) BCL6 RNA Genómica Funcional e Estrutural