The present study aimed to investigate whether rhamnetin induced apoptosis in human breast cancer cells and the underlying molecular mechanism of this anti cancer effect. The treatment of MCF-7 cells with rhamnetin was able to significantly inhibit cell proliferation and induce caspase-3/9 activity in a dose-and time-dependent manner, compared with untreated cells. In addition, treatment with rhamnetin was able to significantly promote the expression of p53 protein and microRNA (miR-)34a compared with untreated cells. The treatment with rhamnetin also suppressed the expression of Notch1 protein in MCF-7 cells compared with untreated cells. Subsequently, miR-24a expression was promoted in rhamnetin-treated MCF-7 cells using a miR-34a plasmid. The overexpression of miR-34a was able to significantly inhibit cell viability and induce caspase-3/9 activity in MCF-7 cells following treatment with rhamnetin. Furthermore, the overexpression of miR-34a was able to significantly promote the expression of p53 protein and miR-34a, and suppress the expression of Notch1 protein in rhamnetin-treated MCF-7 cells. Therefore, the results of the present study demonstrated that rhamnetin induced apoptosis in human breast cancer cells via the miR-34a/Notch-1 signaling pathway.
BackgroundThe purpose of this study was to compare the effects of pemetrexed and carboplatin plus bevacizumab (PC + B) versus pemetrexed and carboplatin (PC) in lung adenocarcinoma patients with EGFR non‐T790M mutations after progression on first‐line EGFR‐tyrosine kinase inhibitors (TKIs).MethodsPatients with EGFR‐positive lung adenocarcinoma who had received second‐line PC with or without bevacizumab harboring EGFR non‐T790M mutations after progression on first‐line EGFR‐TKIs between April 2015 and 2017 at Tianjin Medical University Cancer Institute and Hospital were enrolled in the study. The primary endpoint was progression‐free survival and secondary endpoints were overall survival, objective response rate, disease control rate, and safety.ResultsA total of 85 patients were eligible for the study: 55 and 30 cases were enrolled in the PC and PC + B groups, respectively. The median progression‐free survival was prolonged with PC + B compared to PC (median 8.2 vs. 5.1 months; P = 0.037). The objective response rate was improved with PC + B compared to PC (46.7% vs. 25.5%; P = 0.047) and overall survival prolonged with PC + B compared to PC (median 26.3 vs. 19.2 months; P = 0.012). Safety was similar to previous studies of bevacizumab in non‐small cell lung cancer: one patient experienced grade 3 hypertension and proteinuria but did not require the discontinuation of therapy.ConclusionThe addition of bevacizumab to PC was superior to PC alone as second‐line therapy in patients with advanced non‐T90M EGFR‐positive lung adenocarcinoma. However, this result needs to be confirmed by prospective clinical trials.
Abstract. Sophoridine is an alkaloid extracted from Sophora alopecuroides that has extensive pharmacological actions. In the present study, the effect of sophoridine on cell growth of human medulloblastoma and its mechanism were investigated. Human medulloblastoma D283-Med cells were incubated with 0, 0.5, 1 or 2 mg/ml sophoridine for 24, 48 or 72 h. Cell proliferation and cytotoxicity were analyzed using MTT and lactate dehydrogenase assays, respectively. Next, analyses of cell apoptosis and caspase-3/8 activity were performed using flow cytometry or spectrophotometry, respectively. Lastly, the change in FoxM1, TrkB, BDNF, NF-κB and AP-1 expression was investigated using western blot analysis. In the present study, treatment with sophoridine significantly suppressed cell growth and induced apoptosis in human medulloblastoma cells. In addition, sophoridine significantly increased cytotoxicity and caspase-3/8 activity in human medulloblastoma. Finally, it was found that sophoridine suppresses the protein expression of FoxM1, TrkB, BDNF NF-κB and AP-1 in human medulloblastoma cells. The present study suggests that sophoridine suppresses cell growth of human medulloblastoma through the inhibition of the FoxM1, NF-κB and AP-1 signaling pathway.
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