scholarly journals Downregulation of matrix metalloproteinase-2 (MMP-2) utilizing adenovirus-mediated transfer of small interfering RNA (siRNA) in a novel spinal metastatic melanoma model

Author(s):  
Andrew Tsung ◽  
Odysseas Kargiotis ◽  
Chandramu Chetty ◽  
Sajani Lakka ◽  
Meena Gujrati ◽  
...  
2006 ◽  
Vol 5 (9) ◽  
pp. 2289-2299 ◽  
Author(s):  
Chandramu Chetty ◽  
Praveen Bhoopathi ◽  
Pushpa Joseph ◽  
Subramanyam Chittivelu ◽  
Jasti S. Rao ◽  
...  

2009 ◽  
Vol 11 (1) ◽  
pp. 92-99 ◽  
Author(s):  
Hanna Hlawaty ◽  
Aurélie San Juan ◽  
Marie-Paule Jacob ◽  
Roger Vranckx ◽  
Didier Letourneur ◽  
...  

Endoscopy ◽  
2014 ◽  
Vol 46 (06) ◽  
pp. 507-512 ◽  
Author(s):  
Eun-Young Kim ◽  
Ji Shin ◽  
Ho-Young Song ◽  
Jin Kim ◽  
Edward Lee ◽  
...  

Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 773-781 ◽  
Author(s):  
Lin Yu ◽  
Chun-Yu Wang ◽  
Jiandang Shi ◽  
Lin Miao ◽  
Xiaoling Du ◽  
...  

Accumulating evidence suggests an enhancing effect of estrogens on prostate cancer (PCa) progression. Matrix metalloproteinase 2 (MMP2), which plays an important role in prostate cancer invasion, is mainly expressed in prostatic stromal cells (PrSC). Here we show that estradiol (E2) treatment up-regulates MMP2 production in PrSC, which promotes PCa cell invasion in a paracrine manner. Conditioned medium (CM) was collected from E2-treated prostatic stromal cell line WPMY-1 and primary PrSC. The CM of E2-treated WPMY-1 and PrSC promoted invasion of PCa cells, as measured by Matrigel transwell assays. Treatment with E2 and 1,3,5-Tris(4-hydroxyphenyl)-4-propyl-1H-pyrazole, an estrogen receptor-alpha (ERα) specific agonist, significantly up-regulated MMP2 expression in WPMY-1 and PrSC cells at both mRNA and protein levels. The CM treated with an anti-MMP2 antibody lost the stimulatory effect on invasion of PCa cells. The ER inhibitor ICI 182,780, as well as a TGFβ1 neutralizing antibody and ERα-specific small interfering RNA effectively suppressed E2-induced MMP2 expression in WPMY-1 cells. Mechanistic studies showed that E2 up-regulated MMP2 in an indirect manner: E2 induced TGFβ1 expression via ERα; TGFβ1 stimulated MMP2 expression in PrSC; the invasion of PCa cells were stimulated by elevated MMP2 expression induced by E2 in a paracrine manner. Our data show that E2 induces MMP2 expression in WPMY-1 and PrSC cells, which was mediated by TGFβ1. The effect of E2 on invasion of PCa cells is mediated by up-regulation of MMP2 in a paracrine mechanism.


Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769592 ◽  
Author(s):  
Reza Mohammadzadeh ◽  
Mojgan Saeid Harouyan ◽  
Seyed Mansour Ale Taha

Background: Recently experimental validation of the networks revealed bach1, a basic leucine zipper transcription factor, as the common regulator of several functional invasive genes. The expression of bach1 and its target genes was linked to the higher risk of breast cancer recurrence in patients. The aim of this study was to investigate the effect of specific bach1 small interfering RNAs, on the invasive and expression level of miR-203, miR-145, matrix metalloproteinase-9, and CXCR4 receptor which play a role in cancer metastasis, in MDA-MB-468 cell lines. Methods: Small interfering RNA transfection was performed with transfection regent. The survival effects of small interfering RNA were determined using trypan blue assay cells. The expression level of messenger RNA and matrix metalloproteinase-9 to assess cell invasion and the expression level of miR-203, miR-145, and CXCR4 receptor were measured by quantitative real-time polymerase chain reaction analysis on the MDA-MB-468 cell lines. Results: Transfection with small interfering RNA significantly suppressed the expression of bach1 gene in dose-dependent manner after 48 h ( p < 0.0001). A significant reduction in cell invasion and CXCR4 receptor, matrix metalloproteinase-9 expression were observed ( p < 0.0001). It was also a dramatic increase in the expression level of miR-203 and miR-145 ( p < 0.0001). Conclusions: Our results suggest that the bach1-specific small interfering RNA effectively decrease CXCR4 receptor, matrix metalloproteinase-9 expression and breast adenocarcinoma cells invasive, also increased the expression of tumor-suppressive microRNA-203 and miR-145. Thus, these microRNAs may play a role in invasive/metastasis of carcinogenic breast cancer cells. Therefore, bach1 knockdown can be considered as a potent adjuvant in breast cancer therapy.


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