YY1 and NFYA: Potential tr-KIT Specific Transcription Factors in Prostate Cancer

Objective: Via the use of an alternative promoter, a truncated c-KIT protein (tr-KIT) 30-50 kDa is generated, lacking extracellular and transmembrane domains. Moreover, over-expression tr-KIT, stronger activator than c-KIT, appears to be specific prostate cancer (PCa). Also, Imatinib, tyrosine kinase inhibitor, blocks activity full-length but has no effect on tr-KIT in PCa. Tr-KIT its own nuclear factor binding site. However, transcription factors (TFs) this region are not known yet. This study was conducted define most potential TFs for via silico analysis.Methods: TF sequence uploaded into Tfsitescan database. Five with highest were selected. Transcriptomic data LNCaP (PCa expressing tr-KIT), PC3 tr-KIT) RWPE-1 (normal prostate) cell lines (GSM1647378, GSE36022 GSM738189, respectively) from Gene Expression Omnibus (GEO) database compared gene expression levels pre-defined using DESeq package R-program. Finally, two having higher both detected.Results: selected as: YY1, c-MYB, IL8, NFYA TCF3. analysis performed, it found that YY1 have PCa, among them.Conclusion: may take role formation