الفهرس 
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Abstract
Cancer treatment by natural compounds has emerged as a new approach. The present study firstly aimed to investigate the apoptosis inducing function and potential molecular mechanism of phenethylisothiocyanate (PEITC) and fisetin. Also, study the potential outcome of combining PEITC with Dox or fisetin with Dox on tumor growth and development both in vivo and in vitro.The study found that PEITC acts via multiple molecular targets to elicit anti-carcinogenic activity. The results established that PEITC suppresses the growth of EAT and EAC in vivo, also that fisetin suppresses growth of EAT in vivo and both of them suppresses growth of EAC, breast and hepatoma cells in vitro. PEITC or fisetin were able to induce apoptosis, exert antioxidant effects in addition to inhibition of cell migration. Moreover, PEITC or fisetin use in combination with Dox was able to decrease oxidative stress level caused by Dox treatment alone. The anti-tumor effect as a result of combining PEITC and Dox treatment was superior as compared to fisetin/Dox combination treatment. Thus, PEITC/Dox combination treatment might be used as a potential novel strategy, which may benefit patients with breast and liver cancers.The second part of this study aimed to investigate the role of Unc45A in breast and prostate cancer tumorigenesis and to understand the molecular mechanism by which Unc45A regulates breast and prostate cancer cell proliferation.Unc45A was able to selectively regulate Nek7 transcription in cancer cells, resulting in selective promotion of cancer cell survival and proliferation. This selective function of Nek7 in cancer cells involves differential subcellular localization of Nek7 in normal versus malignant epithelial cells. This difference in localization results in profound functional differences for Unc45A in normal versus malignant cells. In malignant cells, Unc45A has the capacity to regulate Nek7 expression indirectly, via transcriptional co-activation of GR. The present study suggests for the first time a potential therapeutic advantage in targeting Unc45A to block cancer cell proliferation while preserving Nek7 expression and function (cell proliferation) in normal cells.