Modulation of JNK1 MAPK by ATP in osteoblasts and breast cancer cells involvement of mechanical stress activated (SAC) calcium influx

Bone ◽  
2007 ◽  
Vol 40 (3) ◽  
pp. S2
Author(s):  
P Scodelaro Bilbao ◽  
S Katz ◽  
G Santillán
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Mechanical Stress ◽  
Breast Cancer Cells ◽  
Calcium Influx

scholarly journals Mechano-Sensitive Ion Channels (MSCS) Provide Human Breast Cancer Cells with a Sensorium for Mechanical Stress

2014 ◽  
Vol 106 (2) ◽  
pp. 549a-550a
Author(s):  
Chouyang Li ◽  
Simin Rezania ◽  
Sarah Kammerer ◽  
Astrid Gorischek ◽  
Thomas Bauernhofer ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Ion Channels ◽  
Cancer Cells ◽  
Mechanical Stress ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast

scholarly journals Mechanical stress-induced cell death in breast cancer cells

Biology Open ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. bio043133 ◽  
Author(s):  
Satomi Takao ◽  
Minoru Taya ◽  
Cerwyn Chiew
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Mechanical Stress ◽  
Breast Cancer Cells

scholarly journals Compressive Stress Enhances Invasive Phenotype of Breast Cancer Cells via Piezo1 Activation

2019 ◽  
Author(s):  
Mingzhi Luo ◽  
Kenneth KY Ho ◽  
Zhaowen Tong ◽  
Linhong Deng ◽  
Allen Liu
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Compressive Stress ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Calcium Influx ◽  
Breast Cancer Metastasis ◽  
Matrix Degradation ◽  
Apical Side ◽  
Actin Protrusions

Abstract Uncontrolled growth in solid tumor generates compressive stress that drives cancer cells into invasive phenotypes, but little is known about how such stress affects the invasion and matrix degradation of cancer cells and the underlying mechanisms. Here we show that compressive stress enhanced invasion and matrix degradation of breast cancer cells. We further identified Piezo1 as the putative mechanosensitive cellular component that transmits compressive stress to induce calcium influx, which in turn activate Src/ERK signaling. Interestingly, we observed actin protrusions with matrix degradation ability on the apical side of the cells. Furthermore, we demonstrate that Piezo1 channels were partially localized in caveolae, and reduction of caveolin-1 expression or disruption of caveolae with methyl-β-cyclodextrin led to not only reduced Piezo1 expression but also attenuation of the invasive phenotypes promoted by compressive stress. Taken together, our data indicate that mechanical compressive stress activates Piezo1 channels to mediate enhanced cancer cell invasion and matrix degradation that may be a critical mechanotransduction pathway during, and potentially a novel therapeutic target for, breast cancer metastasis.

scholarly journals Compression enhances invasive phenotype and matrix degradation of breast Cancer cells via Piezo1 activation

2022 ◽  
Vol 23 (1) ◽  
Author(s):  
Mingzhi Luo ◽  
Grace Cai ◽  
Kenneth K. Y. Ho ◽  
Kang Wen ◽  
Zhaowen Tong ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Calcium Influx ◽  
Cholesterol Content ◽  
Breast Cancer Metastasis ◽  
Matrix Degradation ◽  
Mechanical Compression ◽  
Invasive Phenotype

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.

scholarly journals Activation of the Ion Channel TRPV4 Induces Epithelial to Mesenchymal Transition in Breast Cancer Cells

2020 ◽  
Vol 21 (24) ◽  
pp. 9417
Author(s):  
Iman Azimi ◽  
Mélanie Robitaille ◽  
Kaela Armitage ◽  
Choon Leng So ◽  
Michael J. G. Milevskiy ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Ion Channel ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Calcium Influx ◽  
Association Studies ◽  
Direct Role ◽  
Mesenchymal Transition ◽  
Emt Markers

Epithelial to mesenchymal transition (EMT) in cancer is important in therapeutic resistance and invasiveness. Calcium signaling is key to the induction of EMT in breast cancer cells. Although inhibition of specific calcium-permeable ion channels regulates the induction of a sub-set of EMT markers in breast cancer cells, it is still unclear if activation of a specific calcium channel can be a driver for the induction of EMT events. In this study, we exploited the availability of a selective pharmacological activator of the calcium-permeable ion channel TRPV4 to assess the direct role of calcium influx in EMT marker induction. Gene association studies revealed a link between TRPV4 and gene-ontologies associated with EMT and poorer relapse-free survival in lymph node-positive basal breast cancers. TRPV4 was an important component of the calcium influx phase induced in MDA-MB-468 breast cancer cells by the EMT inducer epidermal growth factor (EGF). Pharmacological activation of TRPV4 then drove the induction of a variety of EMT markers in breast cancer cells. These studies demonstrate that calcium influx through specific pathways appears to be sufficient to trigger EMT events.

scholarly journals High salt induces P-glycoprotein mediated treatment resistance in breast cancer cells through store operated calcium influx

Oncotarget ◽  
2018 ◽  
Vol 9 (38) ◽  
pp. 25193-25205 ◽  
Author(s):  
Duaa Babaer ◽  
Suneetha Amara ◽  
Michael Ivy ◽  
Yan Zhao ◽  
Philip E. Lammers ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Calcium Influx ◽  
Treatment Resistance ◽  
High Salt ◽  
P Glycoprotein

scholarly journals EHD2 is a mechanotransducer connecting caveolae dynamics with gene transcription

2018 ◽  
Vol 217 (12) ◽  
pp. 4092-4105 ◽  
Author(s):  
Stéphanie Torrino ◽  
Wei-Wei Shen ◽  
Cédric M. Blouin ◽  
Satish Kailasam Mani ◽  
Christine Viaris de Lesegno ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Electron Microscopy ◽  
Gene Regulation ◽  
Plasma Membrane ◽  
Cancer Cells ◽  
Mechanical Stress ◽  
Gene Transcription ◽  
Breast Cancer Cells ◽  
Membrane Tension

Caveolae are small invaginated pits that function as dynamic mechanosensors to buffer tension variations at the plasma membrane. Here we show that under mechanical stress, the EHD2 ATPase is rapidly released from caveolae, SUMOylated, and translocated to the nucleus, where it regulates the transcription of several genes including those coding for caveolae constituents. We also found that EHD2 is required to maintain the caveolae reservoir at the plasma membrane during the variations of membrane tension induced by mechanical stress. Metal-replica electron microscopy of breast cancer cells lacking EHD2 revealed a complete absence of caveolae and a lack of gene regulation under mechanical stress. Expressing EHD2 was sufficient to restore both functions in these cells. Our findings therefore define EHD2 as a central player in mechanotransduction connecting the disassembly of the caveolae reservoir with the regulation of gene transcription under mechanical stress.

The proliferation of breast cancer cells are inhibited by the human intrabody targeting cyclinD1

2010 ◽  
Vol 34 (8) ◽  
pp. S49-S49
Author(s):  
Lei Wang ◽  
Xun Zhou ◽  
Lihong Zhou ◽  
Yong Chen ◽  
Xun Zhu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells
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