PIEZO channel protein naturally expressed in human breast cancer cell MDA-MB-231 as probed by atomic force microscopy

Weng, Yuanqi; Yan, Fei; Chen, Runkang; Qian, Ming; Ou, Yun; Xie, Shuhong; Zheng, Hairong; Li, Jiangyu

doi:10.1063/1.5025036

Cited by 12 publications

(6 citation statements)

References 28 publications

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“…Piezo is highly conserved and has already been linked to a large number of mechanically sensitive processes (23,24,29,30,(61)(62)(63)(64). Following this Dictyostelium precedent, we see no reason why many other types of migrating cell should not also sense their mechanical environment through Piezo.…”

Section: Discussionmentioning

confidence: 94%

Pressure sensing through Piezo channels controls whether cells migrate with blebs or pseudopods

Srivastava

Traynor

Piel

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Blebs and pseudopods can both power cell migration, with blebs often favored in tissues, where cells encounter increased mechanical resistance. To investigate how migrating cells detect and respond to mechanical forces, we used a “cell squasher” to apply uniaxial pressure to Dictyostelium cells chemotaxing under soft agarose. As little as 100 Pa causes a rapid (<10 s), sustained shift to movement with blebs rather than pseudopods. Cells are flattened under load and lose volume; the actin cytoskeleton is reorganized, with myosin II recruited to the cortex, which may pressurize the cytoplasm for blebbing. The transition to bleb-driven motility requires extracellular calcium and is accompanied by increased cytosolic calcium. It is largely abrogated in cells lacking the Piezo stretch-operated channel; under load, these cells persist in using pseudopods and chemotax poorly. We propose that migrating cells sense pressure through Piezo, which mediates calcium influx, directing movement with blebs instead of pseudopods.

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Section: Discussionmentioning

confidence: 94%

Pressure sensing through Piezo channels controls whether cells migrate with blebs or pseudopods

Srivastava

Traynor

Piel

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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“…In the latter case, the role of Piezo channels is even substantiated by the fact that the survival time of the breast cancer patients is negatively related to the mRNA expression level of Piezo1 in the primary tumor [ 18 ]. Interestingly, it has been shown that the response of breast cancer cells to compression is dependent on Piezo but not TRP channels [ 19 ]. And upon activation of Piezo channels (Piezo1 in particular), the corresponding calcium influx evokes several downstream signaling pathways including Src and extracellular regulated protein kinase (ERK) which in turn affect the dynamics of actin-based protrusion structures such as invadopodia/invadosomes that degrade ECM proteins and thus promote invasion [ 20 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

Compression enhances invasive phenotype and matrix degradation of breast cancer cells via Piezo1 activation

Luo

Cai

et al. 2022

BMC Mol and Cell Biol

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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.

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“…One candidate is the piezo channel reported in both MDCK ( 58 ) and HEK293T cells ( 59 ). However, piezo channels are not sensitive to SKF96365 ( 60 ), which inhibited transient induction ( Fig. 4 , C and D ).…”

Section: Discussionmentioning

confidence: 95%

Optogenetic control of small GTPases reveals RhoA mediates intracellular calcium signaling

Inaba

Miao

Nakata

2021

Journal of Biological Chemistry

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Rho/Ras family small GTPases are known to regulate numerous cellular processes, including cytoskeletal reorganization, cell proliferation, and cell differentiation. These processes are also controlled by Ca 2+ , and consequently, cross talk between these signals is considered likely. However, systematic quantitative evaluation has not yet been reported. To fill this gap, we constructed optogenetic tools to control the activity of small GTPases (RhoA, Rac1, Cdc42, Ras, Rap, and Ral) using an improved light-inducible dimer system (iLID). We characterized these optogenetic tools with genetically encoded red fluorescence intensity-based small GTPase biosensors and confirmed these optogenetic tools’ specificities. Using these optogenetic tools, we investigated calcium mobilization immediately after small GTPase activation. Unexpectedly, we found that a transient intracellular calcium elevation was specifically induced by RhoA activation in RPE1 and HeLa cells. RhoA activation also induced transient intracellular calcium elevation in MDCK and HEK293T cells, suggesting that generally RhoA induces calcium signaling. Interestingly, the molecular mechanisms linking RhoA activation to calcium increases were shown to be different among the different cell types: In RPE1 and HeLa cells, RhoA activated phospholipase C epsilon (PLCε) at the plasma membrane, which in turn induced Ca 2+ release from the endoplasmic reticulum (ER). The RhoA–PLCε axis induced calcium-dependent nuclear factor of activated T cells nuclear translocation, suggesting that it does activate intracellular calcium signaling. Conversely, in MDCK and HEK293T cells, RhoA–ROCK–myosin II axis induced the calcium transients. These data suggest universal coordination of RhoA and calcium signaling in cellular processes, such as cellular contraction and gene expression.

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PIEZO channel protein naturally expressed in human breast cancer cell MDA-MB-231 as probed by atomic force microscopy

Cited by 12 publications

References 28 publications

Pressure sensing through Piezo channels controls whether cells migrate with blebs or pseudopods

Pressure sensing through Piezo channels controls whether cells migrate with blebs or pseudopods

Compression enhances invasive phenotype and matrix degradation of breast cancer cells via Piezo1 activation

Optogenetic control of small GTPases reveals RhoA mediates intracellular calcium signaling

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