金丝桃素通过外源性/内源性途径诱导细胞凋亡，并抑制膀胱癌中 NF-κB 调节的生存和侵袭潜能。
Hyperforin Induces Apoptosis Through Extrinsic/Intrinsic Pathways and Inhibits NF-ĸB-modulated Survival and Invasion Potential in Bladder Cancer.
机构信息
Department of Medical Imaging and Radiological Sciences, Central Taiwan University of Science and Technology, Taichung, Taiwan, R.O.C.
Department of Radiation Oncology, Show Chwan Memorial Hospital, Changhua, Taiwan, R.O.C.
出版信息
In Vivo. 2019 Nov-Dec;33(6):1865-1877. doi: 10.21873/invivo.11680.
BACKGROUND/AIM: Muscle-invasive bladder cancer (MIBC) has long been recognized as a difficult to treat cancer type, thus a new treatment strategy is needed. The major purpose of the present study was to verify the anticancer effect of hyperforin and the mechanism through which it affects tumor cell growth and invasion in bladder cancer in vitro.
MATERIALS AND METHODS
Bladder cancer TSGH-8301 cells were treated with different concentrations of hyperforin for different durations of time. The changes in cell viability, production of calcium and reactive oxygen species (ROS), and anti-apoptotic signaling were evaluated using MTT assay, flow cytometry, and western blot analysis. The effect of hyperforin on the expression of nuclear factor-kappaB (NF-ĸB) p65 (Ser276), tumor progression-associated proteins, as well as on cell invasion was investigated using western blotting and cell invasion assay, respectively.
RESULTS
Hyperforin significantly induces apoptosis, extrinsic/intrinsic apoptotic signaling, accumulation of cytosol ROS, and calcium signalling. Hyperforin also significantly diminishes the expression of NF-ĸB p65 (Ser276), anti-apoptotic and tumor progression-associated proteins, as well as the cell invasion ability of TSGH-8301 cells.
CONCLUSION
Our findings demonstrate that hyperforin triggers apoptosis depending on extrinsic/intrinsic pathways and suppresses NF-ĸB-mediated cell survival as well as the invasive properties of bladder cancer in vitro.
背景/目的：肌层浸润性膀胱癌（MIBC）一直被认为是一种难以治疗的癌症类型，因此需要新的治疗策略。本研究的主要目的是验证贯叶金丝桃素在体外对膀胱癌的抗癌作用及其影响肿瘤细胞生长和侵袭的机制。
材料和方法
用不同浓度的贯叶金丝桃素处理膀胱癌 TSGH-8301 细胞不同时间。用 MTT 检测法、流式细胞术和 Western blot 分析评估细胞活力、钙和活性氧（ROS）的产生以及抗凋亡信号的变化。用 Western blot 和细胞侵袭试验分别研究贯叶金丝桃素对核因子-κB（NF-ĸB）p65（Ser276）、肿瘤进展相关蛋白的表达以及细胞侵袭的影响。
结果
贯叶金丝桃素显著诱导细胞凋亡、外源性/内源性凋亡信号、细胞质 ROS 和钙信号的积累。贯叶金丝桃素还显著降低 NF-ĸB p65（Ser276）、抗凋亡和肿瘤进展相关蛋白的表达，以及 TSGH-8301 细胞的侵袭能力。
结论
我们的研究结果表明，贯叶金丝桃素通过外源性/内源性途径触发细胞凋亡，并抑制 NF-ĸB 介导的细胞存活以及体外膀胱癌的侵袭特性。
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