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10.21037/tgh.2018.06.04 http://scihub22266oqcxt.onion/10.21037/tgh.2018.06.04 C6044036!6044036 !30050996     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30050996 &cmd=llinks): Failed to open stream: HTTP request failed! 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Deregulation of methionine metabolism as determinant of progression and prognosis of hepatocellular carcinoma |pdf=|usr=}}{{30050996 }} gab.com Text Deregulation of methionine metabolism as determinant of progression and prognosis of hepatocellular carcinoma JO: Transl Gastroenterol Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=30050996 #FOAvip The under-regulation of liver-specific MAT1A gene codifying for S-adenosylmethionine (SAM) synthesizing isozymes MATI/III, and the up-regulation of widely expressed MAT2A, MATII isozyme occurs in hepatocellular carcinoma (HCC). MAT?1:MAT?2 switch strongly contributes to the fall in SAM liver content both in rodent and human liver carcinogenesis. SAM administration to carcinogen-treated animals inhibits hepatocarcinogenesis. The opposite occurs in Mat1a-KO mice, in which chronic SAM deficiency is followed by HCC development. This review focuses upon the changes, induced by the MAT?1:MAT?2 switch, involved in HCC development. In association with MAT?1:MAT?2 switch there occurs, in HCC, global DNA hypomethylation, decline of DNA repair, genomic instability, and deregulation of different signaling pathways such as overexpression of c-MYC (avian myelocytomatosis viral oncogene homolog), increase of polyamine (PA) synthesis and RAS/ERK (Harvey murine sarcoma virus oncogene homolog/extracellular signal-regulated kinase), IKK/NF-kB (I-k kinase beta/nuclear factor kB), PI3K/AKT, and LKB1/AMPK axes. Furthermore, a decrease in MAT?1 expression and SAM level induces HCC cell proliferation and survival. SAM treatment in vivo and enforced MAT?1 overexpression or MAT?2 inhibition, in cultured HCC cells, prevent these changes. A negative correlation of MAT?1:MAT?2 and MATI/III:MATII ratios with cell proliferation and genomic instability and a positive correlation with apoptosis and global DNA methylation are present in human HCC. Altogether, these data suggest that the decrease of SAM level and the deregulation of MATs are potential therapeutic targets for HCC. Twit Text FOAVip Deregulation of methionine metabolism as determinant of progression and prognosis of hepatocellular carcinoma ????Transl Gastroenterol Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=30050996 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30050996 #FOAvip English Wikipedia <ref>{{Cite pmid|30050996 }}</ref> Deregulation of methionine metabolism as determinant of progression and prognosis of hepatocellular carcinoma #MMPMID30050996 Pascale RM ; Feo CF ; Calvisi DF ; Feo F Transl Gastroenterol Hepatol 2018[]; 3 (ä): 36 PMID30050996 show ga The under-regulation of liver-specific MAT1A gene codifying for S-adenosylmethionine (SAM) synthesizing isozymes MATI/III, and the up-regulation of widely expressed MAT2A, MATII isozyme occurs in hepatocellular carcinoma (HCC). MAT?1:MAT?2 switch strongly contributes to the fall in SAM liver content both in rodent and human liver carcinogenesis. SAM administration to carcinogen-treated animals inhibits hepatocarcinogenesis. The opposite occurs in Mat1a-KO mice, in which chronic SAM deficiency is followed by HCC development. This review focuses upon the changes, induced by the MAT?1:MAT?2 switch, involved in HCC development. In association with MAT?1:MAT?2 switch there occurs, in HCC, global DNA hypomethylation, decline of DNA repair, genomic instability, and deregulation of different signaling pathways such as overexpression of c-MYC (avian myelocytomatosis viral oncogene homolog), increase of polyamine (PA) synthesis and RAS/ERK (Harvey murine sarcoma virus oncogene homolog/extracellular signal-regulated kinase), IKK/NF-kB (I-k kinase beta/nuclear factor kB), PI3K/AKT, and LKB1/AMPK axes. Furthermore, a decrease in MAT?1 expression and SAM level induces HCC cell proliferation and survival. SAM treatment in vivo and enforced MAT?1 overexpression or MAT?2 inhibition, in cultured HCC cells, prevent these changes. A negative correlation of MAT?1:MAT?2 and MATI/III:MATII ratios with cell proliferation and genomic instability and a positive correlation with apoptosis and global DNA methylation are present in human HCC. Altogether, these data suggest that the decrease of SAM level and the deregulation of MATs are potential therapeutic targets for HCC. äDeregulation of methionine metabolism as determinant of progression an(epmc).pdf DeepDyve Pubget Overpricing