Inhibition of cell proliferation by 2-fluorobenzaldehyde retinoic acid conjugate through suppression of STAT3 activation in human glioma cells

被引：0
作者：
Hao, Ji-Heng [1 ,2 ,3 ]
Hu, Dian-Feng [2 ,3 ]
Mao, Li-Mei [4 ,5 ]
Zhang, Shi-Gang [2 ,3 ]
Wang, Ji-Yue [2 ,3 ]
Li, Gang [1 ]
机构：
[1] Shandong Univ, Qilu Hosp, Dept Neurosurg, Jinan 250012, Shandong, Peoples R China
[2] Taishan Med Univ, Liaocheng Peoples Hosp, Dept Neurosurg, Liaocheng 252000, Shandong, Peoples R China
[3] Taishan Med Univ, Liaocheng Clin Sch, Liaocheng 252000, Shandong, Peoples R China
[4] Taishan Med Univ, Liaocheng Peoples Hosp, Dept Hlth, Liaocheng 252000, Shandong, Peoples R China
[5] Taishan Med Univ, Liaocheng Clin Sch, Liaocheng 252000, Shandong, Peoples R China
来源：
BANGLADESH JOURNAL OF PHARMACOLOGY | 2015年 / 10卷 / 04期
关键词：
MYELOMA CELLS; GENE-THERAPY; CANCER CELLS; APOPTOSIS; TRANSCRIPTION; GLIOBLASTOMA; EXPRESSION; TARGETS; GROWTH; TUMORS;
D O I：
10.3329/bjp.v10i4.24165
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
The present study was performed to investigate the effect of 2-fluorobenzaldehyde retinoic acid conjugate on activation of STAT3 pathway in human glioma cells. The results revealed that the compound exhibited inhibitory effect on the activation of STAT3 induced constitutively and by interleukin-6. The inhibitory effect on STAT3 activation was found to be concentration-and time-dependent. In U373 glioma cells, 2-fluorobenz-aldehyde retinoic acid conjugate treatment caused a significant enhancement in the expression of proapoptotic proteins like Bax and Bak. Its treatment inhibited the expression of genes including, cyclin D1, Bcl-2, Bcl-xL, survivin, Mcl-1, and vascular endothelial growth factor (VEGF) in U373 glioma cells. Furthermore, the conjugate inhibited proliferation, induced apoptosis and caused accumulation of cells in G1-G0 phase of cell cycle. Thus, 2-fluorobenzaldehyde retinoic acid conjugate acts as a potent inhibitor of STAT3 activation that can be promising importance for the prevention and treatment of gliomas.
引用
收藏
页码：966 / 971
页数：6
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