ArticleExperimental and therapeutic medicine2019
TAF-Iβ deficiency inhibits proliferation and promotes apoptosis by rescuing PP2A and inhibiting the AKT/GSK-3β pathway in leukemic cells.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Human TAF-Iα promotes oncogenic transformation via enhancement of cell proliferation and suppression of apoptosis.In vitro cellular & developmental biology. Animal · 2021Article
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4 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Template-activating factor Iβ (TAF-Iβ) has been associated with numerous pathophysiological processes and has been reported as an oncogene responsible for the regulation of important signaling pathways in various types of solid tumor; however, few studies have investigated the role of TAF-Iβ in leukemia. The present study reported the upregulated expression of TAF-Iβ in 36 patients with acute leukemia and six leukemic cell lines. In addition, TAF-Iβ-knockdown (KD) cells were generated via RNA interference. TAF-Iβ KD not only inhibited the proliferation of leukemia cells but also induced apoptosis. Furthermore, it was revealed that the mechanism underlying these effects may be associated with the upregulation of protein phosphatase type 2A and inhibition of the protein kinase B/glycogen synthase kinase-3β signaling pathway. Collectively, the findings demonstrated that TAF-Iβ serves an important role in various types of leukemia and may be considered as a potential therapeutic target for the treatment of leukemia.
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