SPARC gene deletion protects against toxic liver injury and is associated to an enhanced proliferative capacity and reduced oxidative stress response

Peixoto, Estanislao; Atorrasagasti, Catalina; Malvicini, Mariana; Fiore, Esteban; Rodríguez, Marcelo M.; Garcı́a, Mariana; Finocchieto, Paola; Poderoso, Juan José; Corrales, Fernando J.; Mazzolini, Guillermo

doi:10.18632/oncotarget.9456

Cited by 3 publications

(2 citation statements)

References 49 publications

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“…It was also demonstrated that Smoc2 was necessary for DNA synthesis in response to PDGF and other growth factors during the cell cycle[39-41]. Our study demonstrated that Smoc2 had a promotive effect on HCC cell G1/S phase progression, as well as on cell proliferation.…”

Section: Discussionsupporting

confidence: 61%

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Su¹,

Kuai²,

Li³

2016

WJG

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AIMTo determine the influence of Smoc2 on hepatocellular carcinoma (HCC) cell proliferation and to find a possible new therapeutic target for preventing HCC progression.METHODSWe detected expression of Smoc2 in HCC tissues and corresponding non-tumor liver (CNL) tissues using PCR, western blot, and immunohistochemistry methods. Subsequently, we down-regulated and up-regulated Smoc2 expression using siRNA and lentivirus transfection assay, respectively. Then, we identified the effect of Smoc2 on cell proliferation and cell cycle using CCK-8 and flow cytometry, respectively. The common cell growth signaling influenced by Smoc2 was detected by western blot assay.RESULTSThe expression of Smoc2 was significantly higher in HCC tissues compared with CNL tissues. Overexpression of Smoc2 promoted HCC cell proliferation and cell cycle progression. Down-regulation of Smoc2 led to inhibition of cell proliferation and cell cycle progression. Smoc2 had positive effect on ERK and AKT signaling.CONCLUSIONSmoc2 promotes the proliferation of HCC cells through accelerating cell cycle progression and might act as an anti-cancer therapeutic target in the future.

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Section: Discussionsupporting

confidence: 61%

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Su¹,

Kuai²,

Li³

2016

WJG

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“…Acute hepatic injury (ALI) leads to a lethal condition if the pathogenic factors are not removed. Hepatic damage is induced by many irritants including chemicals, viruses, infections and other hepatotoxic agents [1,2]. Despite the many mechanisms involved in hepatocyte damage oxidative injury caused by free radicals and reactive oxygen species (ROS) is leading pathogenesis in ALI [3].…”

Section: Introductionmentioning

confidence: 99%

Tert-butylhydroquinone mitigates Carbon Tetrachloride induced Hepatic Injury in mice

Zhang

et al. 2020

Int. J. Med. Sci.

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Tert-butylhydroquinone (tBHQ) is an antioxidant compound that exhibits cytoprotective effect in many tissues under pathological condition. However, its role in carbon tetrachloride (CCL4) induced liver injury is still unclear. Here we established a carbon tetrachloride induced hepatic injury model in mice to determine whether tBHQ can mitigate CCL4 induced liver damage. In our study, we found tBHQ exhibited protective effects in CCL4 treated mice model. TBHQ markedly improved hepatic function and decreased hepatic histopathological damage in vivo. In addition, tBHQ reduced levels of pro-inflammatory cytokines in mice model. Moreover, tBHQ mitigated apoptosis of hepatocytes, oxidative stress and lipid peroxidation in vivo and in vitro. We also found the possible mechanism of protective effects of tBHQ was associated with activation of Nrf2/ heme oxygenase-1 (HO-1) pathway. In conclusion, our study revealed tBHQ can be a potential therapeutic drug in treatment of acute hepatic injury.

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SPARC Controls Migration and Invasion of Hepatocellular Carcinoma Cells Via Regulating GPD2-Mediated Mitochondrial Respiration

Liu,

Xiao,

Yang

2024

Biochem Genet

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SPARC gene deletion protects against toxic liver injury and is associated to an enhanced proliferative capacity and reduced oxidative stress response

Cited by 3 publications

References 49 publications

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Tert-butylhydroquinone mitigates Carbon Tetrachloride induced Hepatic Injury in mice

SPARC Controls Migration and Invasion of Hepatocellular Carcinoma Cells Via Regulating GPD2-Mediated Mitochondrial Respiration

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