Cellular microRNA and the tumorigenesis of hepatocellular carcinoma

Autores: Li Yu, Kowdley Kris V

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Comments Hepatocellular carcinoma (HCC) is one of the most malignant solid tumors causing over 650,000 global deaths each year. Attributed to complex mechanisms, the tumorigenesis of HCC is associated with a broad range of risk factors, including HBV/ HCV infection, heavy alcohol consumption, and non-alcoholic steatohepatitis (NASH). Although the underlying mechanisms of the HCC tumorigenesis is not fully understood, it should be noted that the onset of HCC is often accompanied by inflammation and aberrant proliferation of hepatocytes stimulated by pro-inflammatory cytokines in the liver. Hence, liver inflammation and deregulated hepatocyte proliferation have been postulated as major contributing factors to the tumorigenesis of HCC. Interestingly, the signal transducer and activator of transcription 3 (STAT3) may play critical roles in HCC tumorigenesis due to its involvement in both processes. The phosphorylation of STAT3, induced by extracellular stimuli such as pro-inflammatory cytokines, results in its subsequent translocation into the nucleus; once in the nucleus, STAT3 regulates the transcription of many genes, some important to tumorigenesis. Notably, STAT3 activation is prevalent in malignant tissues in HCC tumors from patients with poor prognosis, but not in adjacent normal tissues. STAT3 activation is transient in normal cells but is constitutive in cancer cells, suggesting its close association with tumorigenesis. However, it remains unclear how the constitutive activation of STAT3 is maintained throughout the tumorigenesis of HCC.

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2012-02-10   |   370 visitas   |   Evalua este artículo 0 valoraciones

Vol. 11 Núm.2. Marzo-Abril 2012 Pags. 272-274 Ann Hepatol 2012; 11(2)