Baicalein suppresses the proliferation of acute T-lymphoblastic leukemia Jurkat cells by inhibiting the Wnt/β-catenin signaling.
Autor: | Liu, Xiaoping, Liu, Shengcai, Chen, Jiarui, He, Li, Meng, Xiangyu, Liu, Shangqin |
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Předmět: |
FLAVONES
LYMPHOBLASTIC leukemia treatment CANCER cell proliferation LYMPHOCYTES WNT signal transduction CATENINS MESSENGER RNA PHYSIOLOGY THERAPEUTICS PREVENTION ANTINEOPLASTIC agents APOPTOSIS BIOCHEMISTRY CELL division CELLULAR signal transduction CYTOSKELETAL proteins DOSE-effect relationship in pharmacology GENES LYMPHOBLASTIC leukemia PHENOMENOLOGY PROTEINS RNA TIME FLAVANONES PHARMACODYNAMICS |
Zdroj: | Annals of Hematology; Oct2016, Vol. 95 Issue 11, p1787-1793, 7p |
Abstrakt: | 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. [ABSTRACT FROM AUTHOR] |
Databáze: | Complementary Index |
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