Involvement of β-catenin expression in hepatocellular carcinoma prognosis in a cohort of patients undergoing curative treatment.

Background: Hepatocellular carcinoma is a tumor of epithelial origin that arises from the action of different carcinogens on the hepatocytes and has a high worldwide incidence. The prognostic markers of this disease have not been completely established. Mutations in the gene encoding β-catenin are overexpressed in hepatocellular carcinoma.

From Nucleus to Organs: Insights of Aryl Hydrocarbon Receptor Molecular Mechanisms.

The aryl hydrocarbon receptor (AHR) is a markedly established regulator of a plethora of cellular and molecular processes. Its initial role in the detoxification of xenobiotic compounds has been partially overshadowed by its involvement in homeostatic and organ physiology processes. In fact, the discovery of its ability to bind specific target regulatory sequences has allowed for the understanding of how AHR modulates such processes.

Liver regeneration after partial hepatectomy is improved in the absence of aryl hydrocarbon receptor.

The liver is among the few organs having the ability to self-regenerate in response to a severe damage compromising its functionality. The Aryl hydrocarbon receptor (Ahr) is a transcription factor relevant for the detoxification of xenobiotics but also largely important for liver development and homeostasis. Hence, liver cell differentiation is developmentally modulated by Ahr through the controlled expression of pluripotency and stemness-inducing genes.

Aryl hydrocarbon receptor blocks aging-induced senescence in the liver and fibroblast cells.

Aging impairs organismal homeostasis leading to multiple pathologies. Yet, the mechanisms and molecular intermediates involved are largely unknown. Here, we report that aged aryl hydrocarbon receptor-null mice () had exacerbated cellular senescence and more liver progenitor cells.

Aryl Hydrocarbon Receptor: From Homeostasis to Tumor Progression.

Transcription factor aryl hydrocarbon receptor (AHR) has emerged as one of the main regulators involved both in different homeostatic cell functions and tumor progression. Being a member of the family of basic-helix-loop-helix (bHLH) transcriptional regulators, this intracellular receptor has become a key member in differentiation, pluripotency, chromatin dynamics and cell reprogramming processes, with plenty of new targets identified in the last decade. Besides this role in tissue homeostasis, one enthralling feature of AHR is its capacity of acting as an oncogene or tumor suppressor depending on the specific organ, tissue and cell type.

The aryl hydrocarbon receptor promotes differentiation during mouse preimplantational embryo development.

Mammalian embryogenesis is a complex process controlled by transcription factors that regulate the balance between pluripotency and differentiation. Transcription factor aryl hydrocarbon receptor (AhR) regulates OCT4/POU5F1 and NANOG, both essential controllers of pluripotency, stemness and early embryo development. Molecular mechanisms controlling OCT4/POU5F1 and NANOG during embryogenesis remain unidentified.

Loss of Aryl Hydrocarbon Receptor Favors -Driven Non-Small Cell Lung Cancer.

Non-small cell lung adenocarcinoma (NSCLC) bearing mutations is one of the most prevalent types of lung cancer worldwide. Aryl hydrocarbon receptor (AHR) expression varies in human lung tumors and has been associated with either increased or reduced lung metastasis. In the mouse, Ahr also adjusts lung regeneration upon injury by limiting the expansion of resident stem cells.