title: Association between SET expression and glioblastoma cell apoptosis and proliferation.
abstract: Glioblastoma multiforme (GBM) was one of the first cancer types systematically studied at a genomic and transcriptomic level due to its high incidence and aggressivity; however, the detailed mechanism remains unclear, even though it is known that numerous cytokines are involved in the occurrence and development of GBM. The present study aimed to determine whether theSETgene has a role in human glioblastoma carcinogenesis. A total of 32 samples, including 18 cases of glioma, 2 cases of meningioma and 12 normal brain tissue samples, were detected using the streptavidin-peroxidase method through immunohistochemistry. To reduceSETgene expression in U251 and U87MG cell lines, the RNA interference technique was used and transfection with small interfering (si)RNA of theSETgene was performed. Cell apoptosis was detected by flow cytometry, cell migration was examined by Transwell migration assay and cell proliferation was determined by Cell Counting Kit-8. SET, Bcl-2, Bax and caspase-3 mRNA and protein expression levels were detected by reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Positive protein expression of SET was observed in the cell nucleus, with the expression level of SET significantly higher in glioma tissues compared with normal brain tissue (P=0.001). Elevated expression of SET was significantly associated with gender (P=0.002), tumors classified as World Health Organization grade II (P=0.031), III (P=0.003) or IV (P=0.001), and moderately (P=0.031) or poorly differentiated (P=0.001) tumors. Compared with the negative and non-treatment (blank) control cells,SETgene expression was significantly inhibited (P=0.006 and P<0.001), cell apoptosis was significantly increased (P=0.001 and P<0.001), cell proliferation was significantly inhibited (P=0.002 and P=0.015), and cell migration was significantly decreased (P=0.001 and P=0.001) in siRNA-transfected U87MG-SETand U251-SETcells, respectively. In addition, mRNA and protein expression levels of Bcl-2 were significantly inhibited in U87MG-SETand U251-SETcells, while mRNA and protein expression levels of Bax and caspase-3 were significantly increased, compared with the two control groups. Thus, the current data suggests that SET may regulate the proliferation and apoptosis of glioblastoma cells by upregulating Bcl-2, and downregulating Bax and caspase-3.
authors.affiliation: Department of Anatomy, Basic Medical and Forensic Medical Institute, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
authors.forename: Kunyan
authors.initials: K
authors.lastname: He
authors.affiliation: Department of Anatomy, Basic Medical and Forensic Medical Institute, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
authors.forename: Lihong
authors.initials: L
authors.lastname: Shi
authors.affiliation: Department of Anatomy, Basic Medical and Forensic Medical Institute, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
authors.forename: Tingting
authors.initials: T
authors.lastname: Jiang
authors.affiliation: Department of Neurosurgery, The Third People's Hospital of Chengdu, Chengdu, Sichuan 610041, P.R. China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Li
authors.affiliation: Department of Anatomy, Basic Medical and Forensic Medical Institute, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
authors.forename: Yao
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Department of Neurosurgery, The Third People's Hospital of Chengdu, Chengdu, Sichuan 610041, P.R. China.
authors.forename: Chuan
authors.initials: C
authors.lastname: Meng
keywords: SET; cell apoptosis; cell migration; cell proliferation; glioblastoma