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• W2052279807 abstract "Inhibitory guanine nucleotide regulatory protein (Gi-protein) signaling to mitogen activated protein kinases (MAPK's) has recently been linked to cellular proliferation. Our laboratory has previously demonstrated elevated expression and activity of the alpha subunits of Gi-proteins (Gi 1, Gil. 2, Gi3) and MAPK proteins (erkl, erk2, mek2) in human hepatocellular carcinoma (HCC) relative to adjacent non-neoplastic liver. We hypothesized that alpha subunits of Gi-proteins control the growth of primary hepatocellular carcinoma through the MAPK pathway. HepG2, Hep3B and SKHep cells were grown to 75% confluence in MEMct supplemented with 10%FBS. Cells were serum deprived for 72 hours prior to treatment with 5% serum or M7 (direct Gi-protein stimulator) +/pertussis toxin (Gi inhibitor) or NF023 (Gict subunit specific inhibitor). Thymidine incorporation was used as an index of cellular mitogenesis. MAPK activity was determined by measuring erk2 phosphorylation of a MAPK substrate, myelin basic protein. Data is expressed as percent of the quiesced cell response. In HepG2 cells pertussis toxin (100ng/ml) caused a significant decrease in [3H]-thymidine incorporation following serum (850 -+ 78% to 455 _+ 50% of quiesced cells, n=4, p<0.05) and M7 (199-+ 24% to 120-+ 25%, n=4, p<0.05) stimulated mitogenesis; NF023 (101aM) caused a significant decrease in [3Hl-thymidine incorporation following serum (1036 -+ 62% to 673 + 63%, n=4, p<0.05) and M7 (185 +4% to 108-+2%, n=4, P<0.05) stimulated mitogenesis. Furthermore, in HepG2 cells, serum and M7 significantly increased MAPK activity, an effect which was significantly inhibited by pertussis toxin and NF023. These effects of pertussis toxin and NF023 on serum and M7 stimulated MAPK and mitogenesis were mimicked in Hep3B and SKHep cell lines. Inhibition of MAPK activity with PD098059 (IIaM;MEK inhibitor) and apigenin (2.5btM; MAPK inhibitor) resulted in decreased serum and M7 stimulated MAPK activity and mitogenesis confirming the pivotal role of MAPK in HCC mitogenesis. These data demonstrate a functionally significant Gic~-protein linked MAPK pathway in HCC. This finding in conjunction with previous data demonstrating enhanced Gic~ and MAPK expression/activity in HCC are evidence of the important role of Gict-protein-MAPK signaling in the growth regulation of this cancer." @default.
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• W2052279807 date "1998-04-01" @default.
• W2052279807 modified "2023-09-27" @default.
• W2052279807 title "Inhibitory guanine nucleotide proteins regulate human hepatocellular carcinoma growth via a MAPK pathway" @default.
• W2052279807 doi "https://doi.org/10.1016/s0016-5085(98)85427-9" @default.
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