ArticleThe Histochemical journal1998
Co-expression of hepatocyte growth factor and its receptor in human prostate cancer.
Article in The Histochemical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 30 citations in OpenAlex.
- RasGRP3 contributes to formation and maintenance of the prostate cancer phenotype.Cancer research · 2010Article
- Met-Independent Hepatocyte Growth Factor-mediated regulation of cell adhesion in human prostate cancer cells.BMC cancer · 2006Article
- Phenotypic switch from paracrine to autocrine role of hepatocyte growth factor in an androgen-independent human prostatic carcinoma cell line, CWR22R.The American journal of pathology · 2004Article
- The tumour-stromal interaction between intratumoral c-Met and stromal hepatocyte growth factor associated with tumour growth and prognosis in non-small-cell lung cancer patients.British journal of cancer · 2004Article
- Hepatocyte growth factor secreted by prostate-derived stromal cells stimulates growth of androgen-independent human prostatic carcinoma cells.The American journal of pathology · 2000Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocyte growth factor acts differently depending on the organs or tumours involved. It may be produced simultaneously with its receptor, c-Met, in several types of malignant tumour cells and may exercise an autocrine regulation. To analyse the effect of hepatocyte growth factor in human prostate cancer, we conducted immunohistochemistry, in situ hybridization and the reverse transcriptase polymerase chain reaction. The first two techniques revealed the growth factor in prostate cancer cells, and the polymerase chain reaction confirmed this expression. c-Met is expressed in prostate cancer cells, but not in interstitial cells. Hepatocyte growth factor is expressed in interstitial cells, especially in hormone-treated cancer tissue, indicating that the growth factor pathway changes with the hormonal status. Low-grade tumours expressed c-Met at the plasma membrane. Higher grade tumours tended to express it in the cytoplasm, suggesting that the role of c-Met as the hepatocyte growth factor receptor was blocked in higher grade tumours. The relationship between the growth factor and its receptor is thus influenced by hormonal status and differentiation in prostate cancer and is not explained simply in terms of autocrine or paracrine action.
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