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厚朴酚通过诱导细胞凋亡增强多药耐药人癌模型中紫杉醇的疗效。

Honokiol enhances paclitaxel efficacy in multi-drug resistant human cancer model through the induction of apoptosis.

作者信息

Wang Xu, Beitler Jonathan J, Wang Hong, Lee Michael J, Huang Wen, Koenig Lydia, Nannapaneni Sreenivas, Amin A R M Ruhul, Bonner Michael, Shin Hyung Ju C, Chen Zhuo Georgia, Arbiser Jack L, Shin Dong M

机构信息

Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia, United States of America.

Department of Radiation Oncology and Otolaryngology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia, United States of America.

出版信息

PLoS One. 2014 Feb 25;9(2):e86369. doi: 10.1371/journal.pone.0086369. eCollection 2014.

Abstract

Resistance to chemotherapy remains a major obstacle in cancer therapy. This study aimed to evaluate the molecular mechanism and efficacy of honokiol in inducing apoptosis and enhancing paclitaxel chemotherapy in pre-clinical multi-drug resistant (MDR) cancer models, including lineage-derived human MDR (KB-8-5, KB-C1, KB-V1) and their parental drug sensitive KB-3-1 cancer cell lines. In vitro analyses demonstrated that honokiol effectively inhibited proliferation in KB-3-1 cells and the MDR derivatives (IC50 ranging 3.35 ± 0.13 µg/ml to 2.77 ± 0.22 µg/ml), despite their significant differences in response to paclitaxel (IC50 ranging 1.66 ± 0.09 ng/ml to 6560.9 ± 439.52 ng/ml). Honokiol induced mitochondria-dependent and death receptor-mediated apoptosis in MDR KB cells, which was associated with inhibition of EGFR-STAT3 signaling and downregulation of STAT3 target genes. Combined treatment with honokiol and paclitaxel synergistically augmented cytotoxicity in MDR KB cells, compared with treatment with either agent alone in vitro. Importantly, the combined treatment significantly inhibited in vivo growth of KB-8-5 tumors in a subcutaneous model. Tumor tissues from the combination group displayed a significant inhibition of Ki-67 expression and an increase in TUNEL-positive cells compared with the control group. These results suggest that targeting multidrug resistance using honokiol in combination with chemotherapy drugs may provide novel therapeutic opportunities.

摘要

对化疗的耐药性仍然是癌症治疗中的一个主要障碍。本研究旨在评估厚朴酚在临床前多药耐药(MDR)癌症模型中诱导细胞凋亡和增强紫杉醇化疗的分子机制及疗效,这些模型包括谱系衍生的人MDR(KB-8-5、KB-C1、KB-V1)及其亲本药物敏感的KB-3-1癌细胞系。体外分析表明,厚朴酚有效抑制KB-3-1细胞和MDR衍生物的增殖(IC50范围为3.35±0.13μg/ml至2.77±0.22μg/ml),尽管它们对紫杉醇的反应存在显著差异(IC50范围为1.66±0.09 ng/ml至6560.9±439.52 ng/ml)。厚朴酚在MDR KB细胞中诱导线粒体依赖性和死亡受体介导的细胞凋亡,这与抑制EGFR-STAT3信号传导和下调STAT3靶基因有关。与单独使用任何一种药物相比,厚朴酚和紫杉醇联合治疗在体外协同增强了MDR KB细胞的细胞毒性。重要的是,联合治疗在皮下模型中显著抑制了KB-8-5肿瘤的体内生长。与对照组相比,联合治疗组的肿瘤组织显示Ki-67表达显著抑制,TUNEL阳性细胞增加。这些结果表明,使用厚朴酚联合化疗药物靶向多药耐药可能提供新的治疗机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91dc/3934844/0333de5d22bd/pone.0086369.g001.jpg

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