By W.G. Jiang (Editor), R.E. Mansel (Editor)
This publication covers the molecular and mobile facets of melanoma metastasis, and discusses the medical point of micro- and macro-metastases, which bring about the loss of life of the vast majority of sufferers with melanoma. the present version makes an attempt to ascertain the present prestige of the fundamental medical and scientific learn within the quarter, and is a really invaluable reference for clinicians, oncologists, and biologists. it really is meant for undergraduates in addition to postgraduates within the zone of drugs, oncology, and melanoma biology.
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Additional resources for Cancer Metastasis, Molecular and Cellular Mechanisms and Clinical Intervention, Volume 1: Biology and Treatment (Cancer Metastasis - Biology and Treatment)
Klemke showed that inhibition of MAPK by a variety of methods (including drug-induced inhibition of MAPK activity, expression of MAPK antisense or blockade of its upstream activator MEK) resulted in reduced MLCK activity, reduced MLC phospho-rylation and reduced migration. In contrast expression of constitutively active MEK resulted in increased migration in COS7 cells. Thus integrindependent activation of the Ras-MAPK pathway could promote a more migratory phenotype. However, this is not the only integrin-activated signalling pathway which modulates migration.
As mentioned above binding to laminin can activate the RasMAPK pathway via Shc and promote growth of keratinocytes(98) whereas activation of PI3K promoted a more invasive phenotype in carcinoma cells (158). Moreover in the presence of EGF migration may be induced(159). All of these functions may have contributed to the observation that is upregulated during progression toward carcinoma in experimental carcinogenesis in mouse skin (160). In contrast de novo expression of resulted in the in vitro growth inhibition of bladder(161) and colorectal (113) cell lines.
Several integrins promote production of MMPs upon adhesion to their ligands. Thus ligation of regulates expression of MMP1 (collagenase type 1) (176). Huhtala and colleagues reported that when rabbit synovial fibroblasts bound to fibronectin via they increased their mRNA and protein for MMP9 (177). Interestingly if the cells simultaneously adhered to the alternatively spliced CS1 region of fibronectin via then this was antagonistic and MMP9 upregulation was inhibited significantly (177). This appears to be an example of integrin crosstalk where the activity of one integrin modulates the activity of another integrin expressed on the same cell (178).