«上一篇/Previous Article|本期目录/Table of Contents|下一篇/Next Article»

《国际骨科学杂志》[ISSN:1673-7083/CN:31-1952/R]

期数:

2017年02期

页码:

115-120

栏目:

实验研究

出版日期:

2017-05-20

文章信息/Info

Title:

The study of saikosaponin-d promotes apoptosis of osteosarcoma cells

作者:

庄怡富; 干耀恺; 汤亭亭

200011, 上海交通大学医学院附属第九人民医院骨科、上海市骨科内植物重点实验室

Author(s):

ZHUANG Yifu;  GAN Yaokai;  TANG Tingting

Department of Orthopaedic, the Ninth People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai Key Laboratory of Orthopaedic Implants, Shanghai 200011, China

关键词:

骨肉瘤;  柴胡皂苷-d;  细胞凋亡;  核因子-κB/丝裂原活化蛋白激酶信号转导通路;  Bcl-2/Bax

Keywords:

Osteosarcoma;  Saikosaponin-d;  Apoptosis;  NF-κB/MAPK;  Bcl-2/Bax

分类号:

-

DOI:

10.3969/j.issn.1673-7083.2017.02.012

文献标识码:

-

摘要:

目的 探讨柴胡皂苷-d(SS-d)对骨肉瘤Saos-2细胞增殖、凋亡、迁移和侵袭能力的影响,并探讨其作用机制。方法 经不同浓度SS-d处理骨肉瘤Saos-2细胞后,采用八肽胆囊收缩素(CCK-8)法检测骨肉瘤细胞增殖情况,采用流式细胞术检测骨肉瘤细胞凋亡情况,采用Transwell小室法检测骨肉瘤细胞迁移和侵袭能力,最后采用蛋白质免疫印迹(Western blot)法探讨SS-d对核因子-κB(NF-κB)/丝裂原活化蛋白激酶(MAPK)信号转导通路的作用及其下游凋亡相关蛋白的影响。结果 SS-d可呈剂量依赖性地明显抑制骨肉瘤Saos-2细胞的增殖、迁移和侵袭能力(P均<0.05),促进骨肉瘤Saos-2细胞凋亡(P<0.05)。SS-d可抑制p-IκBα和p-p65表达,下调p-Jnk和p-p38表达,进而抑制NF-κB/MAPK信号转导通路激活,促进下游凋亡相关蛋白Bax和裂解活化的半胱氨酸天冬氨酸蛋白酶(cleaved caspase)-3表达,减小Bcl-2/Bax比值,促进骨肉瘤Saos-2细胞凋亡。结论 SS-d可明显抑制骨肉瘤Saos-2细胞增殖、迁移和侵袭,促进骨肉瘤Saos-2细胞凋亡。这一现象与SS-d抑制NF-κB/MAPK信号转导通路激活,减小Bcl-2/Bax比值,促进cleaved caspase-3表达有关。

Abstract:

Objective To investigate the effect of saikosaponin-d(SS-d)on the proliferation, apoptosis, migration and invasion of the osteosarcoma Saos-2 cells, and the related mechanism.Methods Osteosarcoma Saos-2 cells were treated with varying concentrations of SS

参考文献/References

[1] Moore DD, Luu HH. Osteosarcoma[J]. Cancer Treat Res, 2014, 162:65-92.
[2] Friedman MA, Carter SK. The therapy of osteogenic sarcoma: current status and thoughts for the future [J]. J Surg Oncol, 1972,4(5):482-510.
[3] Marcove RC, Mike V, Hajek JV, et al. Osteogenic sarcoma under the age of twenty-one. A review of one hundred and forty-five operative cases [J]. J Bone Joint Surg Am, 1970,52(3):411-423.
[4] Zhou W, Hao M, Du X, et al. Advances in targeted therapy for osteosarcoma[J]. Discov Med, 2014, 17(96):301-307.
[5] Szewczyk M, Lechowski R, Zabielska K. What do we know about canine osteosarcoma treatment? Review[J]. Vet Res Commun, 2015, 39(1):61-67.
[6] Ozaki T, Flege S, Kevric M, et al. Osteosarcoma of the pelvis: experience of the cooperative osteosarcoma study group[J]. J Clin Oncol, 2003, 21(2):334-341.
[7] Botter SM, Neri D, Fuchs B. Recent advances in osteosarcoma[J]. Curr Opin Pharmacol, 2014, 16(1):15-23.
[8] 李晓宇,窦立雯,孙佳惠,等.柴胡皂苷d药理与毒理作用研究进展[J]. 中国药物警戒, 2015, 12(4):207-210.
[9] Xu XH, Li T, Fong CM, et al. Saponins from Chinese medicines as anticancer agents[J]. Molecules, 2016, 21(10):1326.
[10] Fujioka T, Yoshida K, Fujii H, et al. Antiproliferative constituents from umbelliferae plants Ⅵ. new ursane-type saikosaponin analogs from the fruits of bupleurum rotundifolium[J]. Chem Pharm Bull(Tokyo), 2003, 51(4):365-372.
[11] Hsu YL, Kuo PL, Lin CC. The proliferative inhibition and apoptotic mechanism of saikosaponin D in human non-small cell lung cancer A549 cells[J]. Life Sci, 2004, 75(10):1231-1242.
[12] Zhong D, Zhang HJ, Jiang YD, et al. Saikosaponin-d: a potential chemotherapeutics in castration resistant prostate cancer by suppressing cancer metastases and cancer stem cell phenotypes[J]. Biochem Biophys Res Commun, 2016, 474(4):722-729.
[13] Jia X, Dang S, Cheng Y, et al. Effects of saikosaponin-d on syndecan-2, matrix metalloproteinases and tissue inhibitor of metalloproteinases-2 in rats with hepatocellular carcinoma[J]. J Tradit Chin Med, 2012, 32(3):415-422.
[14] Jimi E, Fukushima H. NF-kappaB signaling pathways and the future perspectives of bone disease therapy using selective inhibitors of NF-kappaB[J]. Clin Calcium, 2016, 26(2):298-304.
[15] Ye QF, Zhang YC, Peng XQ, et al. Silencing notch-1 induces apoptosis and increases the chemosensitivity of prostate cancer cells to docetaxel through Bcl-2 and Bax[J]. Oncology letters, 2012, 3(4):879-884.
[16] 汪新媛,田京.骨肉瘤化疗研究进展[J]. 国际骨科学杂志, 2010, 31(3):159-161.
[17] 于秀淳,吴苏稼,王序全,等. 晚期骨肉瘤术后复发三例报道并文献复习 [J]. 中国骨与关节杂志, 2013, 2(9):490-494.
[18] Rauch N, Rukhlenko OS, Kolch W, et al. MAPK kinase signalling dynamics regulate cell fate decisions and drug resistance[J]. Curr Opin Struct Biol, 2016, 41:151-158.
[19] Pereira L, Igea A, Canovas B, et al. Inhibition of p38 MAPK sensitizes tumour cells to cisplatin-induced apoptosis mediated by reactive oxygen species and JNK[J]. EMBO Mol Med, 2013, 5(11):1759-1774.
[20] Kim MS, Lee EJ, Kim HR, et al. p38 kinase is a key signaling molecule for H-ras-induced cell motility and invasive phenotype in human breast epithelial cells[J]. Cancer Res, 2003, 63(17):5454-5461.
[21] Uwagawa T, Yanaga K. Effect of NF-kappaB inhibition on chemoresistance in biliary-pancreatic cancer[J]. Surg Today, 2015, 45(12):1481-1488.
[22] Asmarinah A, Paradowska-Dogan A, Kodariah R, et al. Expression of the Bcl-2 family genes and complexes involved in the mitochondrial transport in prostate cancer cells[J]. Int J Oncol, 2014, 45(4):1489-1496.
[23] Pettersson F, Dalgleish AG, Bissonnette RP, et al. Retinoids cause apoptosis in pancreatic cancer cells via activation of RAR-gamma and altered expression of Bcl-2/Bax[J]. Br J Cancer, 2002, 87(5):555-561.

备注/Memo

备注/Memo:

通信作者: 干耀恺 E-mail: ganyk2004@126.com

常用功能

更新日期/Last Update: 2017-05-20