ArticleOncology letters2017
RKTG overexpression inhibits proliferation and induces apoptosis of human leukemia cells via suppression of the ERK and PI3K/AKT signaling pathways.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Molecular mechanisms of ferroptosis and its roles in leukemia.Frontiers in oncology · 2023Review
- Golgi Complex: A Signaling Hub in Cancer.Cells · 2022Review
- PAQR3 inhibits proliferation and aggravates ferroptosis in acute lymphoblastic leukemia through modulation Nrf2 stability.Immunity, inflammation and disease · 2021Article
- PAQR3 protects against oxygen-glucose deprivation/reperfusion-induced injury through the ERK signaling pathway in N2A cells.Journal of molecular histology · 2020Article
- Characterization of the Golgi scaffold protein PAQR3, and its role in tumor suppression and metabolic pathway compartmentalization.Cancer management and research · 2020Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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