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Histidine-rich calcium binding protein promotes growth of hepatocellular carcinoma in vitro and in vivo.

Liu J, Han P, Li M, Yan W, Liu J, He J, Gong J, Wang Y, Tian D - Cancer Sci. (2015)

Bottom Line: We found that ectopic expression of HRC obviously enhanced proliferation and colony formation, while suppression of HRC exhibited inhibitory effects.These effects may result from the ability of HRC to upregulate cyclinD1 and cyclin-dependent kinase 2 (CDK2) expressions and promote G1/S transition.In addition, blocking ERS using 4-phenylbutyric acid (4-PBA) not only downregulated the expression of PERK, ATF4 and CHOP, but also significantly decreased apoptosis induced by HRC silence, whereas ERS inducer thapsigargin (TG) exerted the opposite effects.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

No MeSH data available.


Related in: MedlinePlus

Histidine-rich calcium binding protein (HRC) contributes to G1/S transition in hepatocellular carcinoma (HCC) cells. (a, b) Cell cycle analysis of treated SMMC-7721 and Sk-hep-1 cells. Left, representative image of flow cytometry analysis. Right, mean ± SD from three independent experiments of the percentages of cells in each cell cycle phase. (c, d) The levels of cyclinD1, cyclinE, CDK2 and CDK4 in treated SMMC-7721 and Sk-hep-1 cells were assessed by RT-qPCR and western blotting. GAPDH was used as a loading control. *P < 0.05, **P < 0.01.
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fig03: Histidine-rich calcium binding protein (HRC) contributes to G1/S transition in hepatocellular carcinoma (HCC) cells. (a, b) Cell cycle analysis of treated SMMC-7721 and Sk-hep-1 cells. Left, representative image of flow cytometry analysis. Right, mean ± SD from three independent experiments of the percentages of cells in each cell cycle phase. (c, d) The levels of cyclinD1, cyclinE, CDK2 and CDK4 in treated SMMC-7721 and Sk-hep-1 cells were assessed by RT-qPCR and western blotting. GAPDH was used as a loading control. *P < 0.05, **P < 0.01.

Mentions: To explore the mechanism of HRC-mediated cell growth, we analyzed the cell cycle of HCC cells. The results showed that ectopic expression of HRC dramatically increased the percentage of cells in the S peak and decreased the percentage of cells in the G1/G0 phase, and HRC silence exerted the opposite effect (Fig.3a,b). Next, we measured the expression of the commonly utilized proliferation markers, cyclinD1, cyclinE, CDK2 and CDK4. Prominent changes in the levels of G1 phase regulators cyclinD1 and CDK2 were noted in HCC cells, but no differences were shown on the expression of cyclinE and CDK4 (Fig.3c,d). Collectively, these results suggest that HRC promotes G1/S transition.


Histidine-rich calcium binding protein promotes growth of hepatocellular carcinoma in vitro and in vivo.

Liu J, Han P, Li M, Yan W, Liu J, He J, Gong J, Wang Y, Tian D - Cancer Sci. (2015)

Histidine-rich calcium binding protein (HRC) contributes to G1/S transition in hepatocellular carcinoma (HCC) cells. (a, b) Cell cycle analysis of treated SMMC-7721 and Sk-hep-1 cells. Left, representative image of flow cytometry analysis. Right, mean ± SD from three independent experiments of the percentages of cells in each cell cycle phase. (c, d) The levels of cyclinD1, cyclinE, CDK2 and CDK4 in treated SMMC-7721 and Sk-hep-1 cells were assessed by RT-qPCR and western blotting. GAPDH was used as a loading control. *P < 0.05, **P < 0.01.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4638025&req=5

fig03: Histidine-rich calcium binding protein (HRC) contributes to G1/S transition in hepatocellular carcinoma (HCC) cells. (a, b) Cell cycle analysis of treated SMMC-7721 and Sk-hep-1 cells. Left, representative image of flow cytometry analysis. Right, mean ± SD from three independent experiments of the percentages of cells in each cell cycle phase. (c, d) The levels of cyclinD1, cyclinE, CDK2 and CDK4 in treated SMMC-7721 and Sk-hep-1 cells were assessed by RT-qPCR and western blotting. GAPDH was used as a loading control. *P < 0.05, **P < 0.01.
Mentions: To explore the mechanism of HRC-mediated cell growth, we analyzed the cell cycle of HCC cells. The results showed that ectopic expression of HRC dramatically increased the percentage of cells in the S peak and decreased the percentage of cells in the G1/G0 phase, and HRC silence exerted the opposite effect (Fig.3a,b). Next, we measured the expression of the commonly utilized proliferation markers, cyclinD1, cyclinE, CDK2 and CDK4. Prominent changes in the levels of G1 phase regulators cyclinD1 and CDK2 were noted in HCC cells, but no differences were shown on the expression of cyclinE and CDK4 (Fig.3c,d). Collectively, these results suggest that HRC promotes G1/S transition.

Bottom Line: We found that ectopic expression of HRC obviously enhanced proliferation and colony formation, while suppression of HRC exhibited inhibitory effects.These effects may result from the ability of HRC to upregulate cyclinD1 and cyclin-dependent kinase 2 (CDK2) expressions and promote G1/S transition.In addition, blocking ERS using 4-phenylbutyric acid (4-PBA) not only downregulated the expression of PERK, ATF4 and CHOP, but also significantly decreased apoptosis induced by HRC silence, whereas ERS inducer thapsigargin (TG) exerted the opposite effects.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

No MeSH data available.


Related in: MedlinePlus