ArticleWorld journal of gastroenterology2003
Study on the mechanism of epidermal growth factor-induced proliferation of hepatoma cells.
Article in World journal of gastroenterology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- How Dysregulated Ion Channels and Transporters Take a Hand in Esophageal, Liver, and Colorectal Cancer.Reviews of physiology, biochemistry and pharmacology · 2021Review
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- An Epitope on EGFR Loading Catastrophic Internalization Serve as a Novel Oncotarget for Hepatocellular Carcinoma Therapy.Cancers · 2020Article
- Hepatic cancer stem cells and drug resistance: Relevance in targeted therapies for hepatocellular carcinoma.World journal of hepatology · 2010Article
- Antitumor effect of Gefitinib, an epidermal growth factor receptor tyrosine kinase inhibitor, combined with cytotoxic agent on murine hepatocellular carcinoma.World journal of gastroenterology · 2005Article
- The ErbB2/Neu/HER2 receptor is a new calmodulin-binding protein.The Biochemical journal · 2004Article
- Effect of O-4-ethoxyl-butyl-berbamine in combination with pegylated liposomal doxorubicin on advanced hepatoma in mice.World journal of gastroenterology · 2004Article
- Protective effect of angelica sinensis polysaccharide on experimental immunological colon injury in rats.World journal of gastroenterology · 2003Article
- FT-IR spectroscopic analysis of normal and cancerous tissues of esophagus.World journal of gastroenterology · 2003Article
- Effects of hydroxyapatite nanoparticles on proliferation and apoptosis of human hepatoma BEL-7402 cells.World journal of gastroenterology · 2003Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimMany growth factors, such as epidermal growth factor (EGF), are associated with the carcinogenesis. EGF plays its role in the proliferation of hepatoma cells through binding with EGF receptor (EGFR) and a series of signal transduction. But the postreceptor pathway is still not clear. In the present experiment, we studied the effect of tyrosine kinase, protein kinase C, Na(+)/H(+) exchange, calmodulin and voltage-dependent Ca(2+) channel on EGF-induced hepatoma cell proliferation.
methodsHepatoma cell line SMMC7721 was cultured in RPMI1640 serum-free medium. In order to study the effect of thyrosine kinase, protein kinase C, Na(+)/H(+) exchange, calmodulin and voltage-dependent Ca(2+) channel on human heptoma cell proliferation induced by epidermal growth factor (EGF), DNA synthesis rate of hepatoma cells was measured by the method of (3)H-TdR incorporation.
resultsEGF (10(-9) M) stimulated the proliferation of heptoma cells significantly ((3)H-TdR incorporation was 1 880+/-281 cpm/well, P<0.05), and this effect was significantly inhibited by tyrosine kinase inhibitor genistein ((3)H-TdR incorporation was 808+/-209 cpm/well, P<0.001). Calmodulin inhibitor W-7, protein kinase C inhibitor H-7 and Na(+)/H(+) exchange inhibitor amiloride individually had significant inhibiting effect on EGF-induced proliferation of hepatoma cells ((3)H-TdR incorporation was 978+/-87.3 cpm/well, 1 241+/-147 cpm/well, 1 380+/-189 cpm/well, respectively, P<0.001, P<0.01, P<0.05), but they all had no effect on the basal level proliferation of cultured hepatoma cells ((3)H-TdR incorporation was 1 284+/-260 cpm/well, 1 179+/-150 cpm/well, 1 392+/-152 cpm/well, respectively, (3)H-TdR incorporation of the control was 1 353+/-175 cpm/well, P>0.05). Voltage-dependent Ca(2+) channel inhibitor verapamil had no inhibition on EGF-induced proliferation of hepatoma cells ((3)H-TdR incorporation was 1 637+/-133 cpm/well, P>0.05), it also had no effect on the basal level proliferation of cultured hepatoma cells ((3)H-TdR incorporation was 1 196+/-112 cpm/well, P>0.05).
conclusionOur data suggest that tyrosine kinase, Ca(2+)-calmodulin-dependent pathway, protein kinase C and Na(+)/H(+) exchange play a critical role in EGF-induced proliferation of hepatoma cells and that the effect of EGF is independent of voltage-dependent Ca(2+) channel.
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