Matrine, a natural product extracted from the root of Sophora flavescens, is a promising alternative drug in different types of cancer. Here, we aimed to investigate the therapeutic effects and underlying molecular mechanisms of matrine on human acute lymphoblastic leukemia (ALL) cell line, CCRF-CEM. Cell viability and IC50 values were determined by WST-1 cell cytotoxicity assay. Cell cycle distribution and apoptosis rates were analyzed by flow cytometry. Expression patterns of 44 selected miRNAs and 44 RNAs were analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) using the Applied Biosystems 7500 Fast Real-Time PCR System. Matrine inhibited cell viability and induced apoptosis of CCRF-CEM cells in a dose-dependent manner. Cell cycle analysis demonstrated that matrine-treated CCRF-CEM cells significantly accumulated in the G0/G1 phase compared with the untreated control cells. hsa-miR-376b-3p (-37.09 fold, p = 0.008) and hsa-miR-106b-3p (-16.67 fold, p = 0.028) expressions were decreased, whereas IL6 (95.47 fold, p = 0.000011) and CDKN1A (140.03 fold, p = 0.000159) expressions were increased after matrine treatment. Our results suggest that the downregulation of hsa-miR-106b-3p leads to the upregulation of target p21 gene, CDKN1A, and plays a critical role in the cell cycle progression by arresting matrine-treated cells in the G0/G1 phase.

lung cancer is one of the most commonly diagnosed cancers and it is associated with high rates of morbidity and mortality. Metastasis and relapse of the tumor depend on the survival and proliferation of lung cancer stem cells (lcScs). The ability to identify cScs may prevent recurrence and lead to more effective treatments. Sirtuins are a group of deacetylases that include seven variants (SirT1-7), with sirtuin 1 (SirT1) being the most intensively investigated. evidence suggests that SIRT1 is both a tumor-suppressor gene and an oncogene. SirT1 can deacetylate the tumor-suppressor protein p53 to decrease its activity. SirT1 activators increase the deacetylation of p53, whereas SirT1 inhibitors can stimulate p53 by inhibiting deacetylation. in the present study, cd44 + and cd133 + -enriched a549 (non-small cell lung cancer) cells collected using the cd44 and cd133 cSc surface markers by fluorescence-activated cell sorting method were treated with SirT1 inhibitors (tenovin-6 and sirtinol) and SirT1 activators (resveratrol and SrT1720), and their effects on apoptosis, as well as the mrna and protein expression of SirT1 and p53 were investigated. of these agents, it was found that resveratrol increased p53 expression by 4.1-fold, decreased SirT1 expression by 0.2-fold, and it was the most potent inducer of apoptosis.