Characterization and comparison of telomere length, telomerase and reverse transcriptase activity and gene expression in human mesenchymal stem cells and cancer cells of various origins
| 详细信息 | 推荐本文 | |
- 作者：Byeong-Gyun Jeon (1)
Basavarajappa Mohana Kumar (1)
Eun-Ju Kang (1)
Sun-A Ock (1)
Sung-Lim Lee (1)
Dae-Oh Kwack (2)
June-Ho Byun (3)
Bong-Wook Park (3)
Gyu-Jin Rho (14) jinrho@gnu.ac.kr - 关键词：Mesenchymal stem cells – ; Cancer cells – ; Telomere length – ; Telomerase activity – ; Reverse transcriptase activity
- 刊名：Cell and Tissue Research
- 出版时间：July 2011
- 出版年：2011
- 期刊代码：30_0302-766X
- 类别：med
- 卷：345
- 期：1
- 页码：149-161
- 数据来源：sp
摘要
We have characterized and compared the telomere length, telomerase, reverse transcriptase (RT) activity and expression of genes implicated in cancer and in pluripotency, in human mesenchymal stem cells (MSCs) derived from dental papilla tissue, umbilical cord matrix and adipose tissue and in cancer cells (MDA-MB-231, U-87 MG, and MCF-7). MRC-5 fetal fibroblasts and adult muscle cells were used as somatic cell controls. Telomere length was significantly (P < 0.05) higher in MSCs and somatic cells (7.2-9.3 kb) than in cancer cell lines (3.9-6 kb). However, the relative telomerase activity (RTA) in the cancer cell lines was significantly (P < 0.05) higher than that of MSCs and somatic cells. RTA tended to be slightly higher in MSCs but no significant differences were observed between some cancer cells and MSCs. However, RTA was not detected in somatic cells. Although differentially displayed, the expression of genes related to cancer (BCL-2, p53, NF-κB, TGF-β, VEGF) and transcription and pluripotency (OCT4, NANOG, STAT3, REX1) were commonly observed in MSCs and cancer cells. Thus, endogenous non-telomerase RTA might be a potential biological marker or regulator among MSCs and cancer cells. Further, by sharing the biological and molecular markers of self-renewal and proliferation with cancer cells, MSCs might play a contributory role as tissue resident stem cells in tumor development.