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J Cancer 2017; 8(7):1284-1291. doi:10.7150/jca.17635 This issue Cite

Research Paper

Preferential Association of Lissencephaly-1 Gene Expression with CD133+ Glioblastoma Cells

Felix Mircea Brehar^{1, 2*✉}, Anca Violeta Gafencu^3*, Violeta Georgeta Trusca³, Elena Valeria Fuior³, Dorel Arsene⁴, Mirela Amaireh², Andrei Giovani², Mircea Radu Gorgan^{1, 2}

1. “Carol Davila” University of Medicine and Pharmacy, 37 Dionisie Lupu Street, 020021 Bucharest, Romania;
2. "Bagdasar-Arseni" Clinical Hospital, Neurosurgery Clinic, 10-12 Berceni Street, 041915 Bucharest, Romania;
3. Institute of Cellular Biology and Pathology, "Nicolae Simionescu", 8 B. P. Hasdeu Street, 050568 Bucharest, Romania;
4. “ Victor Babes” National Institute of Pathology, 99-101 Splaiul Independentei Street, 055096 Bucharest, Romania.
* These authors contributed equally to the research in this paper.

✉ Corresponding author: Felix Mircea Brehar, "Bagdasar-Arseni" Clinical Hospital, Neurosurgery Clinic, 10-12 Berceni Street, Bucharest, 041915, e-mail: felixbreharcom, phone: +40724257549, fax: +40213347350

Abstract

Lissencephaly-1 (Lis1) protein is a dynein-binding protein involved in neural stem cell division, morphogenesis and motility. To determine whether Lis1 is a key factor in glioblastoma, we evaluated its expression and function in CD133+ glioblastoma cells. Global, Lis1 gene expression is similar in glioblastoma and normal samples. Interestingly, immunohistochemistry data indicate increased Lis1 expression colocalized with CD133 in a subset of glioma cells, including the tumor cells with perivascular localization. Lis1 gene expression is increased up to 60-fold in CD133 positive cells isolated from primary cultures of glioblastoma and U87 glioblastoma cell line as compared to CD133 negative cells. To investigate the potential role of Lis1 in CD133+ glioblastoma cells, we silenced Lis1 gene in U87 cell line obtaining shLis1-U87 cells. In shLis1-U87 cell culture we noticed a significant decrease of CD133+ cells fraction as compared with control cells and also, CD133+ cells isolated from shLis1-U87 were two times less adhesive, migratory and proliferative, as compared with control transfected U87 CD133+ cells. Moreover, Lis1 silencing decreased the proliferative capacity of irradiated U87 cells, an effect attributable to the lower percentage of CD133+ cells. This is the first report showing a preferential expression of Lis1 gene in CD133+ glioblastoma cells. Our data suggest a role of Lis1 in regulating CD133+ glioblastoma cells function.

Keywords: Glioblastoma, Lis1, CD133, U87 cell line.

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