+ Site Statistics
+ Search Articles
+ PDF Full Text Service
How our service works
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ Translate
+ Recently Requested

Mechanism of cross talk between tissue factor/active coagulation factor VII and epidermal growth factor receptor signalings in colon cancer cells in culture

Mechanism of cross talk between tissue factor/active coagulation factor VII and epidermal growth factor receptor signalings in colon cancer cells in culture

Beijing Da Xue Xue Bao. Yi Xue Ban 49(6): 931-936

To preliminarily verify the cross talk between tissue factor/active coagulation factor VII (TF/FVIIa) and epidermal growth factor receptor (EGFR) pathways in human colon cancer cells in culture. FVIIa was treated to HT-29 (KRAS-wild type) and LoVo (KRAS-mutant) colon cancer cells to activate TF/FVIIa pathway, qRT-PCR and Western blot were used to detect the expressions of amphiregulin (AREG) and epiregulin (EREG), ligands of EGFR on mRNA and protein levels, respectively. After knocking down expression of TF by TF-targeted siRNA transfection, FVIIa was treated and mRNA expressions of AREG and EREG were detected to see whether the FVIIa-induced effects were dependent on TF. Expressions of mRNA of TF and FVII were detected by qRT-PCR following the activation of EGFR pathway by treatment with epidermal growth factor (EGF) to HT-29 and LoVo cells. After TF/FVIIa pathway was activated, for HT-29 cells, expressions of AREG (on mRNA level) and EREG (both on mRNA and protein level) were significantly down-regulated versus those of control group, gene expressions of AREG and EREG were 0.55±0.09 vs.0.99 ±0.09, 0.67±0.10 vs.1.02±0.02, protein expressions of EREG were 0.54±0.09 vs.1.04±0.13, all P<0.05. For LoVo cells, expressions of AREG (both on mRNA and protein level) and EREG (on protein level) were significantly up-regulated versus those of control group, gene expression of AREG were 1.87±0.39 vs. 0.93±0.23, protein expressions of AREG and EREG were 3.09±0.73 vs.1.11±0.21, 1.53±0.19 vs.0.97±0.23, all P<0.05. The regulating effect of AREG and EREG mRNA expression by FVIIa in HT-29 and LoVo cells could both be partly blocked by knocking down TF expression. For HT-29 cells, activation of EGFR pathway induced no significant TF mRNA expression, FVII mRNA expression was not detected. However,for LoVo cells, activation of EGFR pathway induced significantly higher mRNA expressions of both TF and FVII, expressions were 1.53±0.23 vs.1.00±0.23, 53.20±6.08 vs.1.00±0.15, all P<0.05. In colon cancer cell LoVo, when activated, TF/FVIIa pathway and EGFR pathway could interact through upregulating the other pathway's effectors, and mutant KRAS might play a critical role in the two pathways' cross talk.

Please choose payment method:

(PDF emailed within 1 workday: $29.90)

Accession: 065304903

Download citation: RISBibTeXText

PMID: 29263461

Related references

Heterogeneity of receptor function in colon carcinoma cells determined by cross-talk between type I insulin-like growth factor receptor and epidermal growth factor receptor. Cancer Research 68(19): 8004-8013, 2008

Cross-talk between the Tissue Factor/coagulation factor VIIa complex and the tyrosine kinase receptor EphA2 in cancer. Bmc Cancer 16: 341, 2017

Cross-talk among estrogen receptor, epidermal growth factor, and insulin-like growth factor signaling in breast cancer. Clinical Cancer Research 7(12 Suppl.): 4429s-4435s; Discussion 4411s-4412s, 2002

Cross talk of tumor necrosis factor-alpha and epidermal growth factor through EGF receptor in human microvascular endothelial cells. European Cytokine Network 5(2): 134, 1994

The selective epidermal growth factor receptor tyrosine kinase inhibitor ZD1839 blocks estrogen receptor/growth factor cross-talk implicated in tamoxifen resistance in breast cancer. Proceedings of the American Association for Cancer Research Annual Meeting 43: 1001, 2002

Src-mediated aryl hydrocarbon and epidermal growth factor receptor cross talk stimulates colon cancer cell proliferation. American Journal of Physiology. Gastrointestinal and Liver Physiology 302(9): G1006-G1015, 2012

Effective inhibition of the epidermal growth factor/epidermal growth factor receptor binding by anti-epidermal growth factor antibodies is related to better survival in advanced non-small-cell lung cancer patients treated with the epidermal growth factor cancer vaccine. Clinical Cancer Research 14(3): 840-846, 2008

Epidermal growth factor expression in human colon and colon carcinomas: Anti-sense epidermal growth factor receptor RNA down-regulates the proliferation of human colon cancer cells. International Journal of Cancer 62(6): 661-667, 1995

First epidermal growth factor-like domain of human blood coagulation factor IX is required for its activation by factor VIIa/tissue factor but not by factor XIa. Proceedings of the National Academy of Sciences of the United States of America 91(9): 3574-3578, 1994

Epidermal growth factor receptors and effect of epidermal growth factor on growth of human breast cancer cells in long-term tissue culture. Cancer Research 42(11): 4394-4398, 1982

Parabens and Human Epidermal Growth Factor Receptor Ligand Cross-Talk in Breast Cancer Cells. Environmental Health Perspectives 124(5): 563-569, 2017

Insulin-like growth factor-1 receptor inhibition induces a resistance mechanism via the epidermal growth factor receptor/HER3/AKT signaling pathway: rational basis for cotargeting insulin-like growth factor-1 receptor and epidermal growth factor receptor in hepatocellular carcinoma. Clinical Cancer Research 15(17): 5445-5456, 2009

Cross talk among tyrosine kinase receptors in PC12 cells: desensitization of mitogenic epidermal growth factor receptors by the neurotrophic factors, nerve growth factor and basic fibroblast growth factor. Molecular Biology of the Cell 4(7): 737-746, 1993

(-)-Epigallocatechin gallate and polyphenon E inhibit growth and activation of the epidermal growth factor receptor and human epidermal growth factor receptor-2 signaling pathways in human colon cancer cells. Clinical Cancer Research 11(7): 2735-2746, 2005

Growth factor regulation of the renal cortical tubular cells by epidermal growth factor, insulin-like growth factor-I, acidic and basic fibroblast growth factor, and transforming growth factor-beta in serum free culture. Cell Biology International Reports 13(8): 687-699, 1989