NDLI: RKTG overexpression inhibits proliferation and induces apoptosis of human leukemia cells via suppression of the ERK and PI3K/AKT signaling pathways.

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RKTG overexpression inhibits proliferation and induces apoptosis of human leukemia cells via suppression of the ERK and PI3K/AKT signaling pathways.

Content Provider	Semantic Scholar
Author	Xu, Yingdong Deng, Na Wang, Xiaoou Chen, Yinghui Li, Guiji
Copyright Year	2017
Abstract	Raf kinase trapping to Golgi (RKTG) is reported to be a tumor suppressor in a number of solid tumors due to its negative modulation of the Ras/Raf/mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (ERK) pathways. However, the role of RKTG in the progression of leukemia remains unknown. In the present study, a human leukemia U937 cell line overexpressing RKTG was established, and the effect of RKTG on proliferation, cell cycle and apoptosis of human leukemia cells was analyzed. The results of the present study demonstrated that exogenous overexpression of RKTG significantly inhibited cell proliferation, which was accompanied by cell cycle arrest. Apoptosis assay and Hoechst staining demonstrated that the percentage of apoptotic cells in RKTG overexpressing cells was markedly increased. Furthermore, western blotting showed that RKTG overexpression significantly increased the level of cleaved caspase 3, B-cell lymphoma 2 (Bcl2)-associated X apoptosis regulator and reduced the level of Bcl-2. In addition, the activation of ERK and phosphoinositide 3-kinase (PI3K)/AKT serine/threonine kinase 1 signaling pathways in human leukemia cells was also suppressed by RKTG overexpression. In conclusion, the present study demonstrated the tumor-suppressive effect of RKTG on human leukemia cells, which seem to be partially dependent on the suppression of ERK and PI3K/AKT signaling. Overexpression of RKTG may be a potential therapeutic target for the treatment of leukemia.
Starting Page	965
Ending Page	970
Page Count	6
File Format	PDF HTM / HTML
DOI	10.3892/ol.2017.6182
PubMed reference number	28693259
Journal	Medline
Volume Number	14
Issue Number	1
Journal	Oncology letters
Alternate Webpage(s)	https://tessera.spandidos-publications.com/ol/14/1/965/download
Alternate Webpage(s)	https://doi.org/10.3892/ol.2017.6182
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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