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Retracted : Effect of microRNA‐128 on cisplatin resistance of glioma SHG‐44 cells by targeting JAG1
Author(s) -
Yi DongYe,
Su Qing,
Zhang FangCheng,
Fu Peng,
Zhang Qing,
Cen YongCun,
Zhao HongYang,
Xiang Wei
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26469
Subject(s) - apoptosis , transfection , cisplatin , microbiology and biotechnology , flow cytometry , cell growth , chemistry , microrna , jag1 , cell cycle , cell , glioma , cancer research , biology , signal transduction , biochemistry , chemotherapy , gene , genetics , notch signaling pathway
This current study intends to investigate the effect of microRNA‐128 (miR‐128) on cisplatin (DDP) resistance in glioma SHG‐44 cells. SHG‐44/DDP cells were transfected with miR‐128 antisense oligonucleotide (ASO) and assigned into blank, resistance, NC, anti‐miR‐128, miR‐128 mimic, si‐JAG1, and anti‐miR‐128 + si‐JAG1 groups. qRT‐PCR and Western blotting were employed for determining expression of miR‐128, JAG1, Bax and Bcl‐2. MTT assay, Giemsa staining, and flow cytometry were applied to detect DDP resistance, cellular morphology, and cell cycle, respectively. JAG1 is targeted and negatively regulated by miR‐128. In in vitro experiments, compared with the blank group, the rest groups exhibited declined miR‐28 and Bax expression, lowered cell inhibition rate and apoptosis rate, but elevated JAG1 and Bcl‐2 expression with cells arrested in the S phase. Compared with the resistance group, the anti‐miR‐128 group showed decreasedBax expression along with a lowered cell inhibition rate and apoptosis rate, but increased JAG1 and Bcl‐2 expression with reduced cells arrested in the S phase; while the miR‐128 mimic group showed an opposite trend; the si‐JAG1 group showed decreased Bcl‐2 expression and reduced cells in the S phase. In in vivo experiments, compared with the resistance group, the tumor growth rate, tumor volume, and weight as well as JAG1 expression accelerated in the anti‐miR‐128 group; whereas the miR‐128 mimic and si‐JAG1 groups exhibited an opposite trend. Our findings demonstrated that miR‐128 ASO transfection might down‐regulate the expression of miR‐128 in SHG‐44/DDP and up‐regulate the DDP resistance in SHG‐44/DDP cells, providing a potential treatment target for glioma.