Expression Analysis of BORIS as a Cancer-Testis Gene in Cancerous and Non-Cancerous Cell Lines

Publish Year: 1394
نوع سند: مقاله کنفرانسی
زبان: English
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NASTARANCANSER01_034

تاریخ نمایه سازی: 26 شهریور 1395

Abstract:

BORIS is a paralog of CTCF, a transcription factor that plays a key role in chromatininsulation and genomic imprinting. It is generally accepted that BORIS express only in thetestis and certain malignancies. Therefore BORIS is classified as a cancer testis gene.However, some studies have shown widespread expression of BORIS in normal and cancercell lines, why different studies show different results. In the present study, we analyzed theexpression of BORIS in some mouse non cancer (STO and 3T3) and cancer (CT26 coloncarcinoma and N2A Neuroblastoma) cell lines and also Mouse Embryonic Fibroblasts(MEFs) primary cell culture at mRNA (by RT-qPCR) and protein (by immunocytochemistry)level. RT-qPCR results showed that all examined cell lines express Boris, so state ofcancerous or non-cancerous is not a determining factor for the level of Boris expression. Wealso found that BORIS is not expressed in MEFs. Expression analysis at protein levelconfirmed RT-qPCR results. Primary cells such as MEFs have limited lifespan. After a certainnumber of population doublings, cells undergo the process of senescence and stop dividing.Therefore, they would normally not proliferate indefinitely. On the contrary, immortalized celllines (e.g. STO, 3T3, CT26, and N2A) have evaded normal cellular senescence and haveacquired the ability to proliferate indefinitely. It has been reported that long term maintenanceof hES cells and indefinite division of cancer cells in culture are associated withchromosomal abnormalities such as loss of the q arm of chromosome 16 (the locus of CTCF)and gain of chromosome 20q13 (the genetic location of BORIS) and finally increased thelevels of BORIS expression. We propose that a similar association can be seen in otherimmortalized cell lines (e.g. STO, 3T3,CT26, and N2A) that undergo many rounds of celldivision and probably chromosomal abnormalities.

Authors

Sara Soltanian

Department of Biology, Faculty of Science, Shahid Bahonar University of Kerman, Kerman, Iran