CANCER METASTASIS disruption

W4. Ware, J. L., Growth factor network disruption in prostate cancer progression. Cancer Metastasis Rev. 17,443 147 (1999). 

Weak cytotoxicity against human cancer cells, KB and LoVo (colon adenocarcinoma), after treatment with microcarpalide 1, was also observed with the IC50 values of 50 Xg/mL and 90 Xg/mL, respectively. The ability of microcarpalide I (59) to disrupt microfilaments at subcytotoxic concentrations suggests its usefulness for future cell motility and metastasis studies, since other known microfilament disrupting agents such as cytochalasins are cytotoxic at biologically active concentrations. 

Cadherins. Cadherins are a group of glycoproteins that facilitate Ca2+-dependent cell-cell adhesive interactions.20 When cadherin function is disrupted, the release of a tumor cell can result. It was shown that the aggressive metastasis of undifferentiated epithelial carcinoma cells that had lost cell-cell adhesion could be stopped by transfection with E-cad-herin cDNA.21 Therefore, it was suggested that E-cadherin suppresses metastasis,22 which was further supported by more recent studies that showed the loss of adhesion of human gastric, prostatic, and lung cancer cells was due to the gene mutation of a protein associated with the proper function of cadherin.23... 

Hochreiter AE et al. Telomerase template antagonist GRN163L disrupts telomere maintenance, tumor growth, and metastasis of breast cancer. Clin Cancer Res 2006 12 3184-3192. 

Fortin D, Gendron C, Boudrias M, Garant MP. Enhanced chemotherapy delivery by intraarterial infusion and blood-brain barrier disruption in the treatment of cerebral metastasis. Cancer 2007 109 751-760. 

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