In the past two decades, in addition to hepatoprotective effects, anticancer efficacy of silibinin has been demonstrated in numerous studies conducted in cell culture and animal models of cancer of varying phenotypes. Silibinin has been shown to inhibit the proliferation of human colon cancer cells via the inhibition of cell cycle progression by modulating the levels of cyclins and cyclin-dependent kinases. Various in vitro and in vivo studies have also demonstrated the anticancer efficacy of silibinin against human prostate carcinoma cells. Silibinin has been shown to downregulate PSA secretion as well as to inhibit telomerase activity in human prostate carcinoma LNCaP cells, thereby exerting its anticancer effects. Silibinin has also been reported to inhibit the growth and progression of lung carcinogenesis.
Further, synergistic anticancer effects of silibinin have been observed with conventional chemotherapeutic drugs such as doxorubicin, cisplatin, and carboplatin against human breast carcinoma cells. However, there are conflicting reports for the cancer preventive efficacy of silymarin and silibinin against mammary carcinogenesis. Silymarin was reported to enhance l-methyl-I-nitrosourea -induced mammary carcinogenesis as well as to increase the mammary tumor incidences in MMTV-neu/HER2 transgenic mice.
On the contrary, silibinin treatment was shown to strongly inhibit development of mammary tumors as well as lung metastasis in HER-2/neu transgenic mice. In contrast, another study reported that silibinin treatment has no effect on breast cancer development in the C3 SV40 T, t antigen transgenic multiple mammary adenocarcinoma mouse.
These differences could be related to differences in the models used in these studies as well as to the fact that silymarin has other flavonolignans in addition to silibinin, which might possess weak estrogenic activity. In the case of gliomas, silibinin has been reported to sensitize tumor necrosis factor-related apoptosisinducing ligand -resistant glioma cells to TRAIL-mediated apoptosis.
Anticancer effects of silibinin were also observed in renal cell carcinoma, where oral administration of silibinin was found to suppress the growth of local and metastatic tumors in the xenograft model of renal cell carcinoma by increasing the plasma levels of IGFBP-3, a binding protein for insulinlike growth factor 1. Silibinin has also been reported to exert antimetastatic effects through inhibition of urokinaseplasminogen activator and matrix metalloproteinase-9 and -2 expression involved in invasion and metastasis of cancerous cells. In addition, silibinin has been shown to inhibit the invasion and motility of oral cancer cells. Lastly, silibinin exerts protective effects against UV- and chemical carcinogen/tumor promoter-induced skin carcinogenesis through multiple mechanisms detailed in the following sections.
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