Experimental study of inhibition of tumor cell proliferation by a novel gene SPATA12.
10.3969/j.issn.1672-7347.2012.03.002
- Author:
Zhiwen LIU
1
;
Yiting LIN
;
Xuanming LIU
;
Weiwei YU
;
Yunsheng ZHANG
;
Dan LI
Author Information
1. Department of Life Science, School of Biology, Hunan University, Changsha 410082, China.
- Publication Type:Journal Article
- MeSH:
Cell Line, Tumor;
Cell Proliferation;
Genes, Tumor Suppressor;
Genes, cdc;
HeLa Cells;
Homeodomain Proteins;
genetics;
metabolism;
Humans;
Male;
Testicular Neoplasms;
genetics;
pathology;
Transfection
- From:
Journal of Central South University(Medical Sciences)
2012;37(3):222-227
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the inhibitory role of spermatogenesis-associated gene 12 (SPATA12) on tumor cell proliferation and its possible mechanism.
METHODS:The expression pattern of SPATA12 in testicular tumors was investigated by in situ hybridization analysis using tissue microarrays. The effects of SPATA12 on tumor cell proliferation and colony formation was detected by 3-(4.5-dimethylthiazol-2- yl)-2,5-diphenyl tetrazolium bromide (MTT) assay and colonyforming assays, respectively. The changes of expression level of cell cycle genes in tumor cells were detected by reverse transcription polymerase chain reaction(RTPCR).
RESULTS:In situ hybridization analysis showed that the SPATA12 was highly expressed in normal adult testis, but lacking in testicular tumors such as seminoma. MTT assay and colony-forming assay indicated that the exogenous expression of SPATA12 could suppress both tumor cell proliferation and colony formation. RT-PCR showed that the expression of cyclin A1 gene was markedly suppressed and the level of cyclin D1 was somewhat reduced following SPATA12 transfection. However, no obvious changes were observed in mRNA expression of cyclin B1 or cyclin E1 after SPATA12 transfection.
CONCLUSION:SPATA12 could be an inhibitor during the development of tumor via regulation of cell cycle genes.
