At present, the mechanism of tumor cell signaling, selectively block the tumor cells or paracrine secretion of white signal transduction pathway, the destruction of their self-control mechanisms of growth regulators, is an attractive research focus. The one hand, by blocking growth-promoting factors or growth inhibitors enhance the role of the tumor cell growth slow down or stop, on the other hand can also promote tumor cell differentiation, to restore its normal growth regulatory mechanisms (such as cell suicide A mechanism of apoptosis) and changes in the malignant phenotype. The role of these two aspects can be modulated by selective tumor cell signal transduction systems of different components to achieve. This is the classic cytotoxic 'of anti-cancer drug, compared with a selectivity, drug side effects, free from the impact of drug-resistant cells, etc., especially for advanced tumors or metastatic cancer may have a unique effect, very want to be a new generation of anti-cancer drugs. Therefore, signal transduction mechanisms of tumor cells with the potential value and significance. Signal transduction mode of action of the drug can be selected according to different situations:
In most cases, the normal cell signaling mechanism in cancer cells over-activity or over-expression of the normal signaling molecules (such as gene transformation in cancer cells and the DG can be seen phosphoinositide second messenger molecules such as the number of significant increase). This problem can be partially blocked by excessive activation of cell signal transduction pathway, or overexpression of signaling molecules inhibit the ways in which the tumor cell growth slowed down, until close to the level of normal cells.
In some cases, the tumor cells selectively activate signaling molecules, making the cell signaling an exception. Which is a good example of PKC, PKC isoforms in a variety of different cell and tissue expression, respectively. Therefore, we can use this feature, selective modulation of PKC isoforms in tumor cells. Can be seen in many different tumor vinegar acid kinase receptor over-expression or over-activation, sister of common epithelial tumors overexpressed EGFR family of receptors, the blood cell tumor in the common overexpression of IGFR family receptor, glioma Common PDGFR family of receptor overexpression and so on. Overexpression of these receptors or growth factor receptor over-expression leads to excessive activation, leading to activation of downstream signaling pathways, leading to cell transformation, proliferation and resistance to apoptosis, the cells acquire immortality of, and tumor the occurrence and development are closely related. Therefore, blocking tyrosine kinase receptor signal transduction to inhibit tumor growth.
These are the signal transduction mechanism of tumor cell introduction.
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