scholarly journals Upregulation of CD271 transcriptome in breast cancer promotes cell survival via NFκB pathway

Author(s):  
Nabiha Bashir ◽  
Mehreen Ishfaq ◽  
Kehkashan Mazhar ◽  
Jahangir Sarwar Khan ◽  
Ramla Shahid
2020 ◽  
Vol 17 (6) ◽  
pp. 769-779
Author(s):  
MIGUEL A. FERNÁNDEZ-ROJAS ◽  
JORGE MELENDEZ-ZAJGLA ◽  
VILMA MALDONADO LAGUNAS

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1366
Author(s):  
Russell Hughes ◽  
Xinyue Chen ◽  
Natasha Cowley ◽  
Penelope D. Ottewell ◽  
Rhoda J. Hawkins ◽  
...  

Metastatic breast cancer in bone is incurable and there is an urgent need to develop new therapeutic approaches to improve survival. Key to this is understanding the mechanisms governing cancer cell survival and growth in bone, which involves interplay between malignant and accessory cell types. Here, we performed a cellular and molecular comparison of the bone microenvironment in mouse models representing either metastatic indolence or growth, to identify mechanisms regulating cancer cell survival and fate. In vivo, we show that regardless of their fate, breast cancer cells in bone occupy niches rich in osteoblastic cells. As the number of osteoblasts in bone declines, so does the ability to sustain large numbers of breast cancer cells and support metastatic outgrowth. In vitro, osteoblasts protected breast cancer cells from death induced by cell stress and signaling via gap junctions was found to provide important juxtacrine protective mechanisms between osteoblasts and both MDA-MB-231 (TNBC) and MCF7 (ER+) breast cancer cells. Combined with mathematical modelling, these findings indicate that the fate of DTCs is not controlled through the association with specific vessel subtypes. Instead, numbers of osteoblasts dictate availability of protective niches which breast cancer cells can colonize prior to stimulation of metastatic outgrowth.


2011 ◽  
Vol 17 (7) ◽  
pp. 1741-1752 ◽  
Author(s):  
Elsa Vanhecke ◽  
Eric Adriaenssens ◽  
Stéphanie Verbeke ◽  
Samuel Meignan ◽  
Emmanuelle Germain ◽  
...  

2006 ◽  
Vol 66 (1) ◽  
pp. 393-403 ◽  
Author(s):  
Armelle A. Troussard ◽  
Paul C. McDonald ◽  
Elizabeth D. Wederell ◽  
Nasrin M. Mawji ◽  
Nolan R. Filipenko ◽  
...  

Oncogene ◽  
2001 ◽  
Vol 20 (50) ◽  
pp. 7413-7419 ◽  
Author(s):  
Yuvarani S Kuppumbatti ◽  
Brent Rexer ◽  
Shigeo Nakajo ◽  
Kazuyasu Nakaya ◽  
Rafael Mira-y-Lopez

F1000Research ◽  
2014 ◽  
Vol 3 ◽  
pp. 161 ◽  
Author(s):  
Wen Zhou ◽  
Xiaoxia Zhu

Sustained estrogenic exposure increases the risk and/or the progression of various cancers, including those of the breast, endometrium and ovary. Unexpectedly, physiological level of estrogen together with a novel IKKα inhibitor BAY11-7082 could effectively induce cell apoptosis in ER-positive breast cancer cells, suggesting combining estrogen with IKKα inhibition may be beneficial for breast cancer patients. This opinion article touches upon the dual role estrogen played in inducing cancer cell death and asks whether use of estrogen in combination with IKKα-targeted therapy would be possible reconsider the newly identified crosstalk between ER and NFκB pathway which can be utilized to switch the effects of estrogen on cell death.


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