Publications by authors named "Eva Barrasa"
Recent experimental evidences from cellular systems and from mammalian and non-mammalian animal models highlight novel functions for the aryl hydrocarbon/dioxin receptor (AhR) in maintaining cell differentiation and tissue homeostasis. Notably, AhR depletion stimulates an undifferentiated and pluripotent phenotype likely associated to a mesenchymal transition in epithelial cells and to increased primary tumorigenesis and metastasis in melanoma. In this work, we have used a lung model of epithelial regeneration to investigate whether AhR regulates proper tissue repair by adjusting the expansion of undifferentiated stem-like cells.
View Article and Find Full Text PDFThe aryl hydrocarbon receptor (AhR) has roles in cell proliferation, differentiation and organ homeostasis, including the liver. AhR depletion induces undifferentiation and pluripotency in normal and transformed cells. Here, AhR-null mice (AhR-/-) were used to explore whether AhR controls liver regeneration and carcinogenesis by restricting the expansion of stem-like cells and the expression of pluripotency genes.
View Article and Find Full Text PDFPrevious studies suggested that the aryl hydrocarbon receptor (AhR) contributes to mice reproduction and fertility. However, the mechanisms involved remain mostly unknown. Retrotransposon silencing by Piwi-interacting RNAs (piRNAs) is essential for germ cell maturation and, remarkably, AhR has been identified as a regulator of murine B1-SINE retrotransposons.
View Article and Find Full Text PDFBackground: The dioxin (AhR) receptor can have oncogenic or tumor suppressor activities depending on the phenotype of the target cell. We have shown that AhR knockdown promotes melanoma primary tumorigenesis and lung metastasis in the mouse and that human metastatic melanomas had reduced AhR levels with respect to benign nevi.
Methods: Mouse melanoma B16F10 cells were engineered by retroviral transduction to stably downregulate AhR expression, Aldh1a1 expression or both.
Article Synopsis
- Melanoma is a serious skin cancer with low survival rates, and understanding the role of the dioxin receptor (AhR) in tumor growth and spread is essential for improving treatment and prognosis.
- Research shows that AhR has opposing effects on melanoma depending on where it is expressed: it inhibits tumor growth when present in tumor cells but promotes it when found in the surrounding stroma.
- Knockdown of AhR in melanoma cells increases tumor growth and metastasis, indicating that both the tumor and its microenvironment influence cancer progression, suggesting AhR could serve as a potential marker for melanoma.