| Literature DB >> 27506924 |
Xiaoping Liu1, Shengcai Liu2, Jiarui Chen3, Li He2, Xiangyu Meng4, Shangqin Liu5.
Abstract
Although the response rates of chemotherapy in patients with acute T-lymphoblastic leukemia (T-ALL) have improved significantly, the outcome of these patients is still poor. Previous studies suggested that baicalein could inhibit the growth of several cancers, while its effect on T-ALL cells remains unclear. We used Jurkat cells as an in vitro model of T-ALL. Cell counting kit-8 assay and cytometric analysis with Annexin V-FITC/PI double staining were used to investigate the proliferation and apoptosis of Jurkat cells treated with increasing concentration of baicalein for indicated time. RT-PCR and western blotting was used to test the expression of Wnt/β-catenin associated genes and proteins. In cell viability assay, baicalein could inhibit the proliferation of Jurkat cells both in dose- and time-dependent manners. In cell apoptosis assay, baicalein could stimulate apoptosis of Jurkat cells both in dose- and time-dependent manners. Moreover, we demonstrated that baicalein could down-regulated the mRNA and protein levels of β-catenin and its widely accepted downstream targets (c-Myc, cyclin D1, and Axin2) in dose-dependent manners. These results proved that baicalein might be a potential choice for the treatment of T-ALL.Entities:
Keywords: Baicalein; Jurkat cells; T-ALL; Wnt/β-catenin signaling
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Year: 2016 PMID: 27506924 DOI: 10.1007/s00277-016-2766-z
Source DB: PubMed Journal: Ann Hematol ISSN: 0939-5555 Impact factor: 3.673