Journal article

Publication year: 2007

Pages: 3089-3094

Journal: Oncogene

Volume number: 26

Issue number: 21

ISSN: 0950-9232

eISSN: 1476-5594

DOI Link: https://doi.org/10.1038/sj.onc.1210107

Publisher: Springer Nature [academic journals on nature.com]

Abstract: 
Cystatin M is a potent endogenous inhibitor of lysosomal cysteine proteases. In breast carcinoma, cystatin M expression is frequently downregulated. It has been shown that cystatin M expression suppressed growth and migration of breast cancer cells. We examined the methylation status of the CpG island promoter of cystatin M in four breast cancer cell lines (MDAMB231, ZR75-1, MCF7 and T47D), in 40 primary breast carcinoma and in corresponding normal tissue probes by combined bisulphite restriction analysis. To investigate the effects of cystatin M expression on the growth of breast carcinoma, cystatin M was transfected in T47D. The cystatin M promoter was highly methylated in all four-breast cancer cell lines. Primary breast tumours were significantly more frequently methylated compared to normal tissue samples (60 vs 25%; P=0.006 Fisher's exact test). Treatment of breast cancer cells with 5-aza-2′-deoxycytidine (5-Aza-CdR), reactivated the transcription of cystatin M. Transfection of breast carcinoma cells with cystatin M caused a 30% decrease in colony formation compared to control transfection (P=0.002). Our results show that cystatin M is frequently epigenetically inactivated during breast carcinogenesis and cystatin M expression suppresses the growth of breast carcinoma. These data suggest that cystatin M may encode a novel epigenetically inactivated candidate tumour suppressor gene.

Harvard Citation style: Schagdarsurengin, U., Pfeifer, G. and Dammann, R. (2007) Frequent epigenetic inactivation of cystatin M in breast carcinoma, Oncogene, 26(21), pp. 3089-3094. https://doi.org/10.1038/sj.onc.1210107

APA Citation style: Schagdarsurengin, U., Pfeifer, G., & Dammann, R. (2007). Frequent epigenetic inactivation of cystatin M in breast carcinoma. Oncogene. 26(21), 3089-3094. https://doi.org/10.1038/sj.onc.1210107