Objective: Via the use of an alternative promoter, a truncated c-KIT protein (tr-KIT) of 30-50 kDa is generated, lacking extracellular and transmembrane domains. Moreover, over-expression of tr-KIT, a stronger activator than c-KIT, appears to be specific to prostate cancer (PCa). Also, Imatinib, a tyrosine kinase inhibitor, blocks the activity of full-length c-KIT but has no effect on tr-KIT in PCa. Tr-KIT has its own nuclear factor binding site. However, the transcription factors (TFs) binding to this region specific to tr-KIT are not known yet. This study was conducted to define the most potential TFs specific for tr-KIT via in silico analysis.
Methods: Tr-KIT potential TF binding sequence was uploaded into Tfsitescan database. Five TFs with the highest potential binding to this sequence were selected. Transcriptomic data of LNCaP (PCa expressing tr-KIT), PC3 (PCa not expressing tr-KIT) and RWPE-1 (normal prostate) cell lines (GSM1647378, GSE36022 and GSM738189, respectively) from Gene Expression Omnibus (GEO) database were compared for gene expression levels of pre-defined potential tr-KIT specific TFs using DESeq package of R-program. Finally, two TFs having higher expression levels in both LNCaP and PC3 compared to RWPE-1 and higher expression levels in LNCaP compared to PC3 were detected.
Results: Five TFs having the highest potential were selected as: YY1, c-MYB, IL8, NFYA and TCF3. Via in silico analysis performed, it was found that YY1 and NFYA have the highest potential to be tr-KIT specific TFs in PCa, among them.
Conclusion: YY1 and NFYA TFs may take a role in formation of tr-KIT in PCa.
This study was carried out within the scope of TUBITAK 3501 project, numbered 119Z574.
TÜBİTAK
This study was carried out within the scope of TUBITAK 3501 project, numbered 119Z574.
| Primary Language | English |
|---|---|
| Subjects | Health Care Administration |
| Journal Section | Research articles |
| Authors | |
| Project Number | This study was carried out within the scope of TUBITAK 3501 project, numbered 119Z574. |
| Publication Date | May 31, 2022 |
| Published in Issue | Year 2022 Volume: 8 Issue: 2 |