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Tr-KIT Downstream Regulation by YY1 and NFYA Transcription Factors Knockdown in Prostate Cancer Cells
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DOI：10.1002/gcc.70063.png)
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Abstract
En 中文
Prostate cancer is a common and deadly cancer among men and has been the subject of many patients in its diagnosis and treatment. Imatinib, a tyrosine kinase inhibitor, can slow tumor formation by targeting c-KIT, an oncogenic receptor tyrosine kinase protein over-expressed in PCa cases. However, Imatinib has no effect on tr-KIT, a truncated form of c-KIT, which is over-expressed in PCa and is associated with neoplastic transformation. In this study, it is aimed to answer whether the anti-proliferative efficacy of Imatinib on PCa cells could be enhanced by inhibition of tr-KIT specific transcription factors.
Keywords:
c-KIT
imatinib
prostate cancer
Sam68
tr-KIT
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