scholarly journals Down-regulation of uPA and uPAR by 3,3′-diindolylmethane contributes to the inhibition of cell growth and migration of breast cancer cells

2009 ◽  
Vol 108 (4) ◽  
pp. 916-925 ◽  
Author(s):  
Aamir Ahmad ◽  
Dejuan Kong ◽  
Zhiwei Wang ◽  
Sanila H. Sarkar ◽  
Sanjeev Banerjee ◽  
...  
2016 ◽  
Vol 469 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Shunhua Zhang ◽  
Cong Ma ◽  
Haijie Pang ◽  
Fanpeng Zeng ◽  
Long Cheng ◽  
...  

2010 ◽  
Vol 44 (6) ◽  
pp. 319-329 ◽  
Author(s):  
Feng Fang ◽  
Jiamao Zheng ◽  
Traci L Galbaugh ◽  
Alyson A Fiorillo ◽  
Elizabeth E Hjort ◽  
...  

The effects of prolactin (PRL) during the pathogenesis of breast cancer are mediated in part though Stat5 activity enhanced by its interaction with its transcriptional inducer, the prolyl isomerase cyclophilin B (CypB). We have demonstrated that knockdown of CypB decreases cell growth, proliferation, and migration, and CypB expression is associated with malignant progression of breast cancer. In this study, we examined the effect of CypB knockdown on PRL signaling in breast cancer cells. CypB knockdown with two independent siRNAs was shown to impair PRL-induced reporter expression in breast cancer cell line. cDNA microarray analysis was performed on these cells to assess the effect of CypB reduction, and revealed a significant decrease in PRL-induced endogenous gene expression in two breast cancer cell lines. Parallel functional assays revealed corresponding alterations of both anchorage-independent cell growth and cell motility of breast cancer cells. Our results demonstrate that CypB expression levels significantly modulate PRL-induced function in breast cancer cells ultimately resulting in enhanced levels of PRL-responsive gene expression, cell growth, and migration. Given the increasingly appreciated role of PRL in the pathogenesis of breast cancer, the actions of CypB detailed here are of biological significance.


Phytomedicine ◽  
2019 ◽  
Vol 56 ◽  
pp. 156-164 ◽  
Author(s):  
Martina Daga ◽  
Stefania Pizzimenti ◽  
Chiara Dianzani ◽  
Marie Angele Cucci ◽  
Roberta Cavalli ◽  
...  

PLoS ONE ◽  
2020 ◽  
Vol 15 (8) ◽  
pp. e0237889
Author(s):  
Dariusz Wawrzyniak ◽  
Małgorzata Grabowska ◽  
Paweł Głodowicz ◽  
Konrad Kuczyński ◽  
Bogna Kuczyńska ◽  
...  

2019 ◽  
Vol 20 (20) ◽  
pp. 5063
Author(s):  
Lauana Greicy Tonon Lemos ◽  
Gabriel Mello da Cunha Longo ◽  
Bruna dos Santos Mendonça ◽  
Marcela Cristina Robaina ◽  
Mariana Concentino Menezes Brum ◽  
...  

Drug resistance represents a major issue in treating breast cancer, despite the identification of novel therapeutic strategies, biomarkers, and subgroups. We have previously identified the LQB-223, 11a-N-Tosyl-5-deoxi-pterocarpan, as a promising compound in sensitizing doxorubicin-resistant breast cancer cells, with little toxicity to non-neoplastic cells. Here, we investigated the mechanisms underlying LQB-223 antitumor effects in 2D and 3D models of breast cancer. MCF-7 and MDA-MB-231 cells had migration and motility profile assessed by wound-healing and phagokinetic track motility assays, respectively. Cytotoxicity in 3D conformation was evaluated by measuring spheroid size and performing acid phosphatase and gelatin migration assays. Protein expression was analyzed by immunoblotting. Our results show that LQB-223, but not doxorubicin treatment, suppressed the migratory and motility capacity of breast cancer cells. In 3D conformation, LQB-223 remarkably decreased cell viability, as well as reduced 3D culture size and migration. Mechanistically, LQB-223-mediated anticancer effects involved decreased proteins levels of XIAP, c-IAP1, and Mcl-1 chemoresistance-related proteins, but not survivin. Survivin knockdown partially potentiated LQB-223-induced cytotoxicity. Additionally, cell treatment with LQB-223 resulted in changes in the mRNA levels of epithelial-mesenchymal transition markers, suggesting that it might modulate cell plasticity. Our data demonstrate that LQB-223 impairs 3D culture growth and migration in 2D and 3D models of breast cancer exhibiting different phenotypes.


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