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Bortezomib is a novel proteasome inhibitor, which has been successfully used to treat mantle cell lymphoma and multiple myeloma. However, the direct effects of bortezomib on acute promyelocytic leukaemia (APL) have not been fully investigated. In the present study, the WST-8 assay, western blotting, flow cytometry, monodansylcadaverine staining and transmission electron microscopy were performed. It was demonstrated that bortezomib treatment induced a time- and dose-dependent decrease in the viability of NB4 cells. Bortezomib treatment induced cell apoptosis in NB4 cells, as assessed by Annexin V/propidium iodide analysis, and the detection of cleaved caspase-3, cleaved poly(ADP-ribose) polymerase, Bax and Bcl-2 expression. Furthermore, bortezomib treatment induced autophagy in NB4 cells, as indicated by autophagosome formation, p62 degradation, LC3-I to LC3-II conversion and formation of acidic autophagic vacuoles. Notably, autophagy induced by bortezomib was initiated prior to apoptosis. Inhibition of autophagy by knocking down Beclin-1 expression increased bortezomib-induced apoptosis in NB4 cells. Therefore, the present study revealed that the combination of bortezomib and autophagy inhibition may be a potential treatment strategy for APL. 相似文献
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Lei Yang You-Ling Shi Yan Ma Wei-Wei Ren Guang-Ming Pang Jiao Liu 《APMIS : acta pathologica, microbiologica, et immunologica Scandinavica》2022,130(1):43-52
Krüppel-like factor 16 (KLF16), a member of the Krüppel-like factor (KLF) family, has been extensively investigated in multiple cancer types. However, the role of KLF16 in oral squamous cell carcinoma (OSCC) remains unknown. Thus, we conducted this study to investigate its related mechanism. KLF16 expression in OSCC cell lines was quantified by western blotting. Then, OECM1 and OC3 cells were divided into Blank, siCtrl, siKLF16#1 and siKLF16#2 groups. Subsequently, cell proliferation was detected using 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assays, cell migration and invasion were detected with wound healing and Transwell assays, and cell cycle distribution and cell apoptosis were detected via flow cytometry. KLF16, p21, CDK4, Cyclin D1 and p-Rb expression was detected by western blotting. Finally, xenograft models were established in nude mice to observe the in vivo effects of KLF16 on OSCC. KLF16 protein expression was upregulated in OSCC cells. Compared to the cells in the Blank group, the OECM1 and OC3 cells in the siKLF16#1 group and siKLF16#2 group exhibited a sharp decrease in proliferation but a remarkable increase in apoptosis. Moreover, the proportion of cells in the G0/G1 phase notably increased and that in the S phase decreased, with evident decreases in cell invasion and migration. Moreover, KLF16, cyclin-dependent kinase 4 (CDK4), Cyclin D1 and p-Rb protein expression was upregulated, but p21 expression was downregulated. The mice in the siKLF16#1 and siKLF16#2 xenograft model groups exhibited slower tumour growth and smaller tumours with evident downregulation of Ki67 expression compared to the mice in the Blank group. KLF16 expression was upregulated in OSCC cells, and interfering with KLF16 led to cell cycle arrest, inhibited OSCC cell growth and promoted cell apoptosis. 相似文献
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背景 慢性阻塞性肺疾病(COPD)患者肺栓塞(PE)发生率显著高于常人,但目前不伴红细胞增多的COPD患者并发PE的机制尚不明确。目的 探讨不伴红细胞增多的COPD患者并发PE的影响因素。方法 本研究为回顾性病例对照研究。收集2017年1-12月在新疆医科大学第一附属医院呼吸与呼吸危重症中心住院治疗的血红蛋白(Hb)≤140 g/L的COPD患者。依据肺多层螺旋CT肺血管成像(CTPA)检查结果将患者分为并发PE组和单纯COPD组。记录患者的年龄、性别、合并症、服用抗血小板或抗凝药物史。采用倾向性评分匹配(PSM)方法,通过二元Logistic回归分析估计倾向性评分值,采用1∶1最邻近原则匹配,卡钳值为0.05,筛选出基线相同的两组病例。记录患者的D-二聚体、血常规检查结果,比较两组间差异;分析不伴红细胞增多的COPD患者并发PE的影响因素,红细胞分布宽度(RDW)与中性粒细胞/淋巴细胞比值(NLR)的相关性。结果 共纳入病例339例,其中单纯COPD组289例,并发PE组50例。采用PSM方法筛选两组患者,最终得到单纯COPD组、并发PE组各50例进行后续研究。并发PE组患者D-二聚体、中性粒细胞计数(N)、RDW、NLR高于单纯COPD组,淋巴细胞计数(L)低于单纯COPD组(P<0.05)。二元Logistic回归分析结果显示,RDW是不伴红细胞增多的COPD患者并发PE的影响因素〔OR=1.561,95%CI(1.096,2.225),P<0.05〕。Spearman秩相关分析结果显示,不伴红细胞增多的COPD患者RDW与NLR呈正相关(rs=0.225,P<0.05)。结论 RDW升高是Hb≤140 g/L的COPD患者并发PE的危险因素,且RDW与NLR呈正相关。 相似文献