Hepatocellular carcinoma

Summary

Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer in adults and is currently the most common cause of death in people with cirrhosis. HCC is the third leading cause of cancer-related deaths worldwide. The development of HCC is attributed to fibrosis and cirrhosis, which occur in the setting of chronic liver injury and inflammation. The latter being closely linked to chronic viral hepatitis infection (hepatitis B or C) or exposure to toxins such as alcohol, aflatoxin, or pyrrolizidine alkaloids. Certain diseases, such as hemochromatosis and alpha 1-antitrypsin deficiency, markedly increase the risk of developing HCC. Metabolic syndrome and NASH are also increasingly recognized as risk factors for HCC. As with any cancer, the treatment and prognosis of HCC vary depending on the specifics of tumor histology, size, how far the cancer has spread, and overall health. The vast majority of HCC cases and the lowest survival rates after treat

Official source

https://en.wikipedia.org/wiki/Hepatocellular_carcinoma

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Nuclear receptors play pleiotropic roles in cell differentiation, development, proliferation, and metabolic processes to govern liver physiology and pathology. The nuclear receptor, liver receptor homolog-1 (LRH-1, NR5A2), originally identified in the liver as a regulator of bile acid and cholesterol homeostasis, was recently recognized to coordinate a multitude of other hepatic metabolic processes, including glucose and lipid processing, methyl group sensing, and cellular stress responses. In this review, we summarize the physiological and pathophysiological functions of LRH-1 in the liver, as well as the molecular mechanisms underlying these processes. This review also focuses on the recent advances highlighting LRH-1 as an attractive target for liver-associated diseases, such as non-alcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC).

2021

The identification of cellular pathways capable of limiting ischemia/reperfusion (I/R) injury remains a frontier in medicine, and its clinical relevance is urgent. Histidine triad nucleotide binding protein 1 (HINT1) is a tumor suppressor that influences apoptosis. Because apoptotic pathways are a feature of I/R injury, we asked whether Hint1 influences hepatic I/R injury. Hint1(-/-) and C57BL/6 mice were subjected to 70% liver ischemia followed by reperfusion for 3 or 24 hours or to a sham operation. The serum aminotransferase levels, histological lesions, apoptosis, reactive oxygen species, and expression of B cell lymphoma 2-associated X protein (Bax), heme oxygenase 1 (HO-1), interleukin-6 (IL-6), IL-10, tumor necrosis factor-a, Src, nuclear factor kappa B (p65/RelA), and c-Jun were quantified. The responses to toll-like receptor ligands and nicotinamide adenine dinucleotide phosphate oxidase activity in Kupffer cells were compared in Hint1(-/-) mice and C57BL/6 mice. After I/R, the levels of serum aminotransferases, parenchymal necrosis, and hepatocellular apoptosis were significantly lower in Hint1(-/-) mice versus control mice. Furthermore, Bax expression decreased more than 2-fold in Hint1(-/-) mice, and the increases in reactive oxygen species and HO-1 expression that were evident in wild-type mice after I/R were absent in Hint1(-/-) mice. The phosphorylation of Src and the nuclear translocation of p65 were increased in Hint1(-/-) mice, whereas the nuclear expression of phosphorylated c-Jun was decreased. The levels of the protective cytokines IL-6 and IL-10 were increased in Hint1(-/-) mice. These effects increased survival after I/R in mice lacking Hint1. Hint1(-/-) Kupffer cells were less activated than control cells after stimulation with lipopolysaccharides. Conclusion: The Hint1 protein influences the course of I/R injury, and its ablation in Kupffer cells may limit the extent of the injury. (HEPATOLOGY 2011;53:243-252)

2011

Deciphering the Role of LRH-1 in Liver Intermediary Metabolism and Cancer

Pan Xu

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death worldwide. Gaining insight into the molecular pathways involved in the development of HCC is hence a prerequisite to design and develop novel and effective therapeutic strategies. Metabolic reprogramming is a universal feature of tumor cells and is characterized by increased glycolysis and diminished oxidative phosphorylation, a phenomenon known as the Warburg effect. More recently, it has become evident that tumor cells heavily rely on gluta-mine metabolism to compensate for the Warburg effect and to replenish the tricarboxylic acid (TCA) cycle. However, the molecular mechanisms by which glutamine supports tumor cell metabolism remain largely unexplored. In this thesis, I have established the role of the nuclear receptor LRH-1 as a key regulator in the process of hepatic tumorigenesis. I observed that LRH-1 promotes DEN-induced hepatocellular carcinogenesis (HCC). I demonstrated that LRH-1 facilitates the production of NADPH from glutamine by favoring a non-canonical glutamine pathway that optimizes reductive biosynthesis. Importantly, chronic and acute disrup-tion of LRH-1 also impaired glutamine-induced anaplerosis and Î±-KG availability, ultimately leading to im-paired mTORC1 signaling to block cell proliferation. Moreover, LRH-1 also coordinates glutamine-dependent asparagine synthesis to protect tumor cell from apoptosis induced by glutamine depletion itself. As a result, gain-of-function of LRH-1 sustained aspar-agine homeostasis upon glutamine-deprivation to promote cell survival. Collectively, these studies unveiled an unexpected role of LRH-1 in cancer intermediary metabolism, and warranted further studies on pharma-cological inhibition of LRH-1 to interfere with hepatocellular carcinogenesis.

EPFL2016