Open AccessRNAi‐mediated inhibition of MSP58 decreases tumour growth, migration and invasion in a human glioma cell line
Author(s) -
Lin Wei,
Zhang Jing,
Zhang Jian,
Liu Xinping,
Fei Zhou,
Li Xia,
Davidovic Laetitia,
Tang Zhuo,
Shen Lan,
Deng Yanchun,
Yang Angang,
Han Hua,
Zhang Xiang,
Yao Libo
Publication year - 2009
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2008.00499.x
Subject(s) - biology , gene knockdown , glioma , cancer research , cell cycle , small hairpin rna , cell growth , rna interference , cell culture , cell , microbiology and biotechnology , gene , rna , genetics
MSP58, a 58‐kD nuclear microspherule protein, is an evolutionarily conserved nuclear protein implicated in the regulation of gene transcription as well as in malignant transformation. An analysis of mRNA expression by real‐time PCR revealed that MSP58 was significantly up‐regulated in 29% of high‐grade glioblastoma tissues as well as in four glioblastoma cell lines. In the present study, we further evaluated the biological functions of MSP58 in U251 glioma cell proliferation, migration, invasion and tumour growth in vivo by specific MSP58 knockdown using short hairpin RNA (shRNA). We found that MSP58 depletion inhibited glioma cell growth, primarily by inducing cell cycle arrest rather than apoptosis. MSP58 depletion also decreased the invasive capability of glioma cells and anchorage‐independent colony formation in soft agar. Moreover, suppression of MSP58 expression significantly impaired the growth of glioma xenografts in nude mice. Finally, a cell cycle‐associated gene array revealed potential molecular mechanisms contributing to cell cycle arrest in MSP58‐depleted glioma cells. In summary, our data highlight the importance of MSP58 in glioma progression and provided a biological basis for MSP58 as a novel candidate target for treatment of glioma.