scholarly journals Inhibition of SYK kinase does not confer a pro-proliferative or pro-invasive phenotype in breast epithelium or breast cancer cells

Oncotarget ◽  
2020 ◽  
Vol 11 (14) ◽  
pp. 1257-1272 ◽  
Author(s):  
David J. Lamb ◽  
Aleksander Rust ◽  
Albin Rudisch ◽  
Tobias Glüxam ◽  
Nathalie Harrer ◽  
...  
2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Jason R Dobson ◽  
Hanna Taipaleenmäki ◽  
Yu-Jie Hu ◽  
Deli Hong ◽  
Andre J van Wijnen ◽  
...  

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0131842 ◽  
Author(s):  
Sangeet Lal ◽  
Cymon Kersch ◽  
Kathleen A. Beeson ◽  
Y. Jeffrey Wu ◽  
Leslie L. Muldoon ◽  
...  

BMC Cancer ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Wenjie Deng ◽  
Yueyuan Wang ◽  
Luo Gu ◽  
Biao Duan ◽  
Jie Cui ◽  
...  

2022 ◽  
Vol 23 (1) ◽  
Author(s):  
Mingzhi Luo ◽  
Grace Cai ◽  
Kenneth K. Y. Ho ◽  
Kang Wen ◽  
Zhaowen Tong ◽  
...  

Abstract Background Uncontrolled growth in solid breast cancer generates mechanical compression that may drive the cancer cells into a more invasive phenotype, but little is known about how such compression affects the key events and corresponding regulatory mechanisms associated with invasion of breast cancer cells including cellular behaviors and matrix degradation. Results Here we show that compression enhanced invasion and matrix degradation of breast cancer cells. We also identified Piezo1 as the putative mechanosensitive cellular component that transmitted compression to not only enhance the invasive phenotype, but also induce calcium influx and downstream Src signaling. Furthermore, we demonstrated that Piezo1 was mainly localized in caveolae, and both Piezo1 expression and compression-enhanced invasive phenotype of the breast cancer cells were reduced when caveolar integrity was compromised by either knocking down caveolin1 expression or depleting cholesterol content. Conclusions Taken together, our data indicate that mechanical compression activates Piezo1 channels to mediate enhanced breast cancer cell invasion, which involves both cellular events and matrix degradation. This may be a critical mechanotransduction pathway during breast cancer metastasis, and thus potentially a novel therapeutic target for the disease.


2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Amy L. Strong ◽  
Dorothy T. Pei ◽  
Christian G. Hurst ◽  
Jeffrey M. Gimble ◽  
Matthew E. Burow ◽  
...  

Obesity is associated with enhanced tumor growth and progression. Within the adipose tissue are adipose-derived stromal/stem cells (ASCs) that have been shown to convert into carcinoma-associated fibroblast (CAFs) in the presence of tumor-derived factors. However, the impact of obesity on the ASCs and on the conversion of ASCs into CAFs has not been demonstrated. In the current study, ASCs isolated from lean donors (BMI < 25; lnASCs) were compared with ASCs isolated from obese donors (BMI > 30, obASCs). The contribution of tumor-derived factors on the conversion of ASCs to CAFs was investigated. Following exposure to cancer cells, obASCs expressed higher levels of CAF markers, including NG2, alpha-SMA, VEGF, FAP, and FSP, compared to lnASCs. To investigate the crosstalk between ASCs and breast cancer cells, MCF7 cells were serially cocultured with lnASCs or obASCs. After coculture with lnASCs and obASCs, MCF7 cells demonstrated enhanced proliferation and expressed an invasive phenotype morphologically, with more pronounced effects following exposure to obASCs. Long-term exposure to obASCs also enhanced the expression of protumorgenic factors. Together, these results suggest that obesity alters ASCs to favor their rapid conversion into CAFs, which in turn enhances the proliferative rate, the phenotype, and gene expression profile of breast cancer cells.


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