Brain lipid binding protein mediates the proliferation of human glioblastoma cells by regulating ERK1/2 signaling pathway in vitro

• Published in: In vitro cellular & developmental biology. Animal Vol. 54; no. 2; pp. 156 - 162
• Main Authors: Tian, Wei, Shi, Jinhong, Qin, Jianbing, Jin, Guohua, Han, Xiao, Li, Haoming
• Format: Journal Article
• Language: English
• Published: New York Springer Science & Business Media LLC 01.02.2018; Springer US; Society for In Vitro Biology
• Subjects: Adenoviruses; Animal Genetics and Genomics; Biomedical and Life Sciences; Brain; Brain cancer; Brain research; Cancer; Cell Biology; Cell Culture; Cell growth; CELL GROWTH/DIFFERENTIATION/APOPTOSIS; Cell proliferation; Central nervous system; CRISPR; Deoxyribonucleic acid; Depletion; Developmental Biology; DNA; Extracellular signal-regulated kinase; Fatty acids; Gene expression; Genomes; Glial cells; Glioblastoma cells; Inhibition; Kinases; Life Sciences; Lipids; Nervous system; p53 Protein; Proteins; Radial glial cells; Signal transduction; Stem Cells; CRISPR/Cas9; BLBP; Glioblastoma; U251 cells; P53
• ISSN: 1071-2690; 1543-706X
• DOI: 10.1007/s11626-017-0220-8

Brain lipid binding protein (BLBP) is highly expressed in the radial glial cells (RGCs) of the central nervous system (CNS), in glioblastomas, and, in vitro, in U251 cells. In this report, we have demonstrated that increased BLBP expression in glioblastoma is associated with poor survival and used a double-vector CRISPR/Cas9 lentiviral system to deplete endogenous BLBP from U251 cells, we found that loss of BLBP induced cell growth inhibition and S-phase arrest. Moreover, an increase in P53 and a decrease in p-ERK1/2 were observed after BLBP depletion, suggesting a potential mechanism by which loss of BLBP results in growth inhibition.