Hematoporphyrin and doxorubicin co-loaded nanomicelles for the reversal of drug resistance in human breast cancer cells by combining sonodynamic therapy and chemotherapy

RSC Advances ◽  
2016 ◽  
Vol 6 (102) ◽  
pp. 100361-100372 ◽  
Author(s):  
Guoyun Wan ◽  
Yang Liu ◽  
Shurui Shi ◽  
Bowei Chen ◽  
Yue Wang ◽  
...  

HPDF nanomicells reversed drug resistance of MCF-7/ADR cells by combining sonodynamic therapy and chemotherapy.

Biomaterials ◽  
2014 ◽  
Vol 35 (35) ◽  
pp. 9495-9507 ◽  
Author(s):  
Gan Lin ◽  
Wencheng Zhu ◽  
Li Yang ◽  
Jun Wu ◽  
Bingbing Lin ◽  
...  

2011 ◽  
Vol 10 (1) ◽  
pp. 135 ◽  
Author(s):  
Yusuke Yamamoto ◽  
Yusuke Yoshioka ◽  
Kaho Minoura ◽  
Ryou-u Takahashi ◽  
Fumitaka Takeshita ◽  
...  

2003 ◽  
Vol 17 (10) ◽  
pp. 2002-2012 ◽  
Author(s):  
Olga A. Sukocheva ◽  
Lijun Wang ◽  
Nathaniel Albanese ◽  
Stuart M. Pitson ◽  
Mathew A. Vadas ◽  
...  

Abstract Current understanding of cytoplasmic signaling pathways that mediate estrogen action in human breast cancer is incomplete. Here we report that treatment with 17β-estradiol (E2) activates a novel signaling pathway via activation of sphingosine kinase (SphK) in MCF-7 breast cancer cells. We found that E2 has dual actions to stimulate SphK activity, i.e. a rapid and transient activation mediated by putative membrane G protein-coupled estrogen receptors (ER) and a delayed but prolonged activation relying on the transcriptional activity of ER. The E2-induced SphK activity consequently activates downstream signal cascades including intracellular Ca2+ mobilization and Erk1/2 activation. Enforced expression of human SphK type 1 gene in MCF-7 cells resulted in increases in SphK activity and cell growth. Moreover, the E2-dependent mitogenesis were highly promoted by SphK overexpression as determined by colony growth in soft agar and solid focus formation. In contrast, expression of SphKG82D, a dominant-negative mutant SphK, profoundly inhibited the E2-mediated Ca2+ mobilization, Erk1/2 activity and neoplastic cell growth. Thus, our data suggest that SphK activation is an important cytoplasmic signaling to transduce estrogen-dependent mitogenic and carcinogenic action in human breast cancer cells.


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