2019
DOI: 10.1371/journal.pone.0212860
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Targeting mTOR and Src restricts hepatocellular carcinoma growth in a novel murine liver cancer model

Abstract: Liver cancer is a poor prognosis cancer with limited treatment options. To develop a new therapeutic approach, we derived HCC cells from a known model of murine hepatocellular carcinoma (HCC). We treated adiponectin (APN) knock-out mice with the carcinogen diethylnitrosamine, and the resulting tumors were 7-fold larger than wild-type controls. Tumors were disassociated from both genotypes and their growth characteristics evaluated. A52 cells from APN KO mice had the most robust growth in vitro … Show more

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Cited by 20 publications
(16 citation statements)
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“…Murine primary HCC cells, named A52, that we previously developed 16 , and human HCC Huh7 cells were used to study the effects of HCC growth in glucose and fructose supplemented media. Cells were cultured in glucose or fructose supplemented media and cell proliferation evaluated after 24, 48 and 72 h. Compared to glucose, HCC cells grown in fructose had significantly reduced cell proliferation (p < 0.05; Fig.…”
Section: Resultsmentioning
confidence: 99%
See 1 more Smart Citation
“…Murine primary HCC cells, named A52, that we previously developed 16 , and human HCC Huh7 cells were used to study the effects of HCC growth in glucose and fructose supplemented media. Cells were cultured in glucose or fructose supplemented media and cell proliferation evaluated after 24, 48 and 72 h. Compared to glucose, HCC cells grown in fructose had significantly reduced cell proliferation (p < 0.05; Fig.…”
Section: Resultsmentioning
confidence: 99%
“…Huh7 HCC cells were cultured in DMEM media supplemented with 10% heat-inactivated FBS and 1% (v/v) Penicillin-Streptomycin (Gibco). A52 HCC cells were used for a murine model of HCC as published by us 16 and cultured in DMEM supplemented with 20% heat-inactivated FBS, 20 μg/L human epidermal growth factor (hEGF; Sigma Aldrich), 0.01 g/L insulin (Gibco), 0.01 g/L hydrocortisone, 1 mM phenobarbital, and 1% (v/v) Penicillin-Streptomycin. Cells were maintained at 37 °C in 5% CO 2 .…”
Section: Methodsmentioning
confidence: 99%
“…Recently, our group showed that the formation of foamy macrophages in human NAFLD is mediated by the macrophage scavenger receptor 1, resulting in the release of pro-inflammatory cytokines, such as TNFa, but also inducing metabolic changes in the liver [73,74] . Adiponectin, on the other hand, is regarded as an anti-inflammatory modulator in NAFLD and is protective against HCC formation [69,75] . Though HPCs in NAFLD show a decreased expression of adiponectin, indicative for a shift towards a pro-inflammatory phenotype, they also secrete GLP-1, which can decrease transaminases and reduce intrahepatic triglycerides and macrophage infiltration in a NASH mouse model [44,76] .…”
Section: Hepatic Progenitor Cell Secretomementioning
confidence: 99%
“…However, constitutive activation of Src (which can be promoted by Rap1 activation [74]) has been shown to sustain mTORC1 activity and promotes cell survival under nutrient deprivation conditions [75]. Combinatorial treatment with Src inhibitor (dasatinib) and mTORC1 inhibitor (rapamycin) reduced tumor growth [76]. Hence, these controversial results indicate the need of further studies to validate the role of Rap1 in regulating mTORC1 activity.…”
Section: Rap1 Regulates Autophagy and Cancer Metabolism Via Mtorc1mentioning
confidence: 99%