|Table of Contents|

Docetaxel Down-Regulation of Smad3 Expression in Prostate CancerCell Lines Independent of TGF-β1 Signaling(PDF)

《南京师大学报(自然科学版)》[ISSN:1001-4616/CN:32-1239/N]

Issue:
2016年03期
Page:
89-
Research Field:
·生命科学·
Publishing date:

Info

Title:
Docetaxel Down-Regulation of Smad3 Expression in Prostate CancerCell Lines Independent of TGF-β1 Signaling
Author(s):
Pi YuruiLi TonghuiChen XiubinLiu PingLu Shan
School of Life Sciences,Nanjing Normal University,Jiangsu Key Laboratory for Molecular and Medical Biotechnology,Nanjing 210023,China
Keywords:
docetaxelSmad3prostate cancerdown-regulation
PACS:
Q28
DOI:
10.3969/j.issn.1001-4616.2016.03.015
Abstract:
As a taxane anticancer drug,docetaxel(DOC)derived from the European yew needles has been widely used as the therapies for multiple cancers in clinic though a lot of related mechanism remains unclear. In this study,the DOC regulation of Smad3 expression in the presence of TGF-b signal was first observed in prostate cancer cell line PC-3 level,and then the effects of DOC on cell growth and Smad3 expression in the absence of TGF-b1 signal was investigated in prostate cancer LNCaP cells without TGF-b RII to explore related mechanism mainly by reverse transcription polymerase chain reaction(RT-PCR),Western blot,etc. It was found that DOC not only down-regulated Smad3 mRNA and protein levels in PC-3 cells in a time-and dose-dependent ways,but also selectively reduced Smad3 expression and inhibited cell growth in LNCaP cells while Smad2 expression was not decreased,and DOC also reduced Smad3 expression in PC-3 cells cultured in the absence of TGF-b1. Meanwhile,the Stat1 expressions in both of PC-3 and LNCaP cells were significantly inhibited by DOC. Moreover,Stat1 and Smad3 could bind together to form complex. Besides,it is also speculated that 5 potential binding sites for Stat1 existed from the analysis for Smad3 core promoter region. In total,DOC down-regulation of Smad3 is not depend on the TGF-b1 signaling,and may be caused by affecting Stat1 bindings with Smad3 promoter specific sites.

References:

[1] JAIN A,THAKUR K,KUSH P,et al. Docetaxel loaded chitosan nanoparticles:formulation,characterization and cytotoxicity studies[J]. Int J Biol Macromol,2014,69:546-53.
[2] KOPCZYNSKA E. Role of microRNAs in the resistance of prostate cancer to docetaxel and paclitaxel[J]. Contemp Oncol(Pozn),2016,19(6):423-427.
[3] HORWITZ S B. Mechanism of action of taxol[J]. Trends Pharmacol Sci,1992,13(4):134-136.
[4] HIROSE A,TAJIMA H,OHTA T,et al. Low-dose paclitaxel inhibits the induction of epidermal-mesenchymal transition in the human cholangiocarcinoma CCKS-1 cell line[J]. Oncol Lett,2013,6(4):915-920.
[5] TSUKADA T,FUSHIDA S,HARADA S,et al. Low-dose paclitaxel modulates tumour fibrosis in gastric cancer[J]. Int J Oncol,2013,42(4):1 167-1 174.
[6] WANG C,SONG X,LI Y,et al. Low-dose paclitaxel ameliorates pulmonary fibrosis by suppressing TGF-beta1/Smad3 pathway via miR-140 upregulation[J]. PLoS One,2013,8(8):e70725.
[7] YAO B,ZHAO J,LI Y,et al. Elf5 inhibits TGF-beta-driven epithelial-mesenchymal transition in prostate cancer by repressing SMAD3 activation[J]. Prostate,2015,75(8):872-82.
[8] 刁小伟,李园,皮玉瑞,等. 雄激素依赖性前列腺癌细胞中雄激素受体上调EphA3表达[J]. 天津医药,2015,43(11):1?253-1 257.
[9] 董源,汤灵玲,林林,等. 蛋白含量检测的抗干扰新方法[J]. 生物工程学报,2012,28(9):1 130-1 138.
[10] AREF-ESHGHI E,LIU M,RAZAVI-LOPEZ S B,et al. SMAD3 is upregulated in human osteoarthritic cartilage independent of the promoter DNA methylation[J]. J Rheumatol,2016,43(2):388-394.
[11] LEE J Y,ELMER H L,ROSS K R,et al. Isoprenoid-mediated control of SMAD3 expression in a cultured model of cystic fibrosis epithelial cells[J]. Am J Respir Cell Mol Biol,2004,31(2):234-240.
[12] CENGIZ E,KARACA B,KUCUKZEYBEK Y,et al. Overcoming drug resistance in hormone- and drug-refractory prostate cancer cell line,PC-3 by docetaxel and gossypol combination[J]. Mol Biol Rep,2010,37(3):1 269-1 277.
[13] MOHR A,CHATAIN N,DOMOSZLAI T,et al. Dynamics and non-canonical aspects of JAK/STAT signalling[J]. Eur J Cell Biol,2012,91(6/7):524-532.
[14] YANG Q,WANG Y,LU X,et al. MiR-125b regulates epithelial-mesenchymal transition via targeting Sema4C in paclitaxel-resistant breast cancer cells[J]. Oncotarget,2015,6(5):3 268-3 279.
[15] ZHANG Y,HUANG S. Up-regulation of miR-125b reverses epithelial-mesenchymal transition in paclitaxel-resistant lung cancer cells[J]. J Biol Chem,2015,15(4):45.
[16] ADAMKPVA L,SOUCKOVA K,KOVARIK J,et al. Transcription protein STAT1:biology and relation to cancer[J]. Folia Biol(Praha),2007,53(1):1-6.
[17] RAVEN J F,WILLIAMS V,WANG S,et al. Stat1 is a suppressor of ErbB2/Neu-mediated cellular transformation and mouse mammary gland tumor formation[J]. Cell cycle,2011,10(5):794-804.
[18] KHARMA B,BABA T,MATSUMURA N,et al. STAT1 drives tumor progression in serous papillary endometrial cancer[J]. Cancer Res,2014,74(22):6 519-6 530.
[19] ARZT L,KOTHMAIER H,HALBWEDL I,et al. Signal transducer and activator of transcription 1(STAT1)acts like an oncogene in malignant pleural mesothelioma[J]. Virchows Arch,2014,465(1):79-88.
[20] ZHANG M. Novel function of STAT1 in breast cancer[J]. Oncoimmunology,2013,2(8):e25125.
[21] PATTERSON S G,WEI S,CHEN X,et al. Novel role of Stat1 in the development of docetaxel resistance in prostate tumor cells[J]. Oncogene,2006,25(45):6 113-6 122.

Memo

Memo:
-
Last Update: 2016-09-30