Actin cytoskeleton stiffness grades metastatic potential of ovarian carcinoma Hey A8 cells via nanoindentation mapping

Zhou, Zhuo; Sun, Xinhe; Ma, Jing; Tong, Minghui; To, Sally K Y; Wong, Alice S.T.; Ngan, A.H.W.

doi:10.1016/j.jbiomech.2017.06.040

Cited by 13 publications

(16 citation statements)

References 36 publications

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“…We reasoned that unexpectedly low stiffness of PDCD10 cells might be due to specifics of the architecture of actin cytoskeleton in these cells. Indeed, as demonstrated in previous studies, cells with highly aligned stress fibers had lower overall stiffness when compared with cells with a more intertwined organization of the cytoskeleton ( Zhou et al., 2017 ). To address this possibility, we visualized filamentous actin with fluorescently labeled phalloidin and performed immunocytochemical staining of cultures using antibodies against MLC-P ( Figure 3 E, top row) to study the distribution of actomyosin fibers in WT and KD cells.…”

Section: Resultssupporting

confidence: 67%

Biomechanics of Endothelial Tubule Formation Differentially Modulated by Cerebral Cavernous Malformation Proteins

et al. 2018

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SummaryAt early stages of organismal development, endothelial cells self-organize into complex networks subsequently giving rise to mature blood vessels. The compromised collective behavior of endothelial cells leads to the development of a number of vascular diseases, many of which can be life-threatening. Cerebral cavernous malformation is an example of vascular diseases caused by abnormal development of blood vessels in the brain. Despite numerous efforts to date, enlarged blood vessels (cavernomas) can be effectively treated only by risky and complex brain surgery. In this work, we use a comprehensive simulation model to dissect the mechanisms contributing to an emergent behavior of the multicellular system. By tightly integrating computational and experimental approaches we gain a systems-level understanding of the basic mechanisms of vascular tubule formation, its destabilization, and pharmacological rescue, which may facilitate the development of new strategies for manipulating collective endothelial cell behavior in the disease context.

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Section: Resultssupporting

confidence: 67%

Biomechanics of Endothelial Tubule Formation Differentially Modulated by Cerebral Cavernous Malformation Proteins

et al. 2018

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“…The average healing rates of OVCAR-3 and HO-8910 were significantly greater than that of HOSEpiC (Figure 2a,b), which is consistent with the changes of viscoelastic results by AFM, indicating the relationship between migratory potential and viscoelastic properties of ovarian cancer cells. Zhou et al found that Hey HM cells exhibited a higher migration capacity than NM cells, also indicating that the difference in stiffness in Hey A8 cells with different metastasis potential is related to changes in the cytoskeleton structure, which are similar with our results of this investigation [18]. Additionally, some studies have reported the cells with higher motility were usually associated with lower stiffness [42,43].…”

Section: Tumorigenic Properties Of Ovarian Cancer Cellssupporting

confidence: 90%

“…In addition, stiffness and deformation of cells are strongly regulated by the microfilament skeleton [16]. Therefore, the rearrangement of microfilament skeleton is crucial for cell motility and contributes largely to elasticity changes of the cells, when the cytoskeleton structure changes from a more organized to a disordered form with the transformation from benign to malignant [17,18]. However, the association of viscoelastic properties with the invasion of ovarian cancer cells is not well understood.…”

Section: Introductionmentioning

confidence: 99%

Examination of the relationship between viscoelastic properties and the invasion of ovarian cancer cells by atomic force microscopy

Chen¹,

Zeng²,

Ruan³

et al. 2020

Beilstein J. Nanotechnol.

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The mechanical properties of cells could serve as an indicator for disease progression and early cancer diagnosis. This study utilized atomic force microscopy (AFM) to measure the viscoelastic properties of ovarian cancer cells and then examined the association with the invasion of ovarian cancer at the level of living single cells. Elasticity and viscosity of the ovarian cancer cells OVCAR-3 and HO-8910 are significantly lower than those of the human ovarian surface epithelial cell (HOSEpiC) control. Further examination found a dramatic increase of migration/invasion and an obvious decease of microfilament density in OVCAR-3 and HO-8910 cells. Also, there was a significant relationship between viscoelastic and biological properties among these cells. In addition, the elasticity was significantly increased in OVCAR-3 and HO-8910 cells after the treatment with the anticancer compound echinomycin (Ech), while no obvious change was found in HOSEpiC cells after Ech treatment. Interestingly, Ech seemed to have no effect on the viscosity of the cells. Ech significantly inhibited the migration/invasion and significantly increased the microfilament density in OVCAR-3 and HO-8910 cells, which was significantly related with the elasticity of the cells. An increase of elasticity and a decrease of invasion were found in OVCAR-3 and HO-8910 cells after Ech treatment. Together, this study clearly demonstrated the association of viscoelastic properties with the invasion of ovarian cancer cells and shed a light on the biomechanical changes for early diagnosis of tumor transformation and progression at single-cell level.

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“…Scaffolding proteins embrace molecules such as FN1, plasminogen activator inhibitor 1 (PAI1), collagens, and periostin and composed the ECM network, providing molecular signals and tensional forces that are required to the cell to migrate. The modification in ECM conformation determines changes in physical parameters, such as stiffness and network dimension, that can reveal the clinical diagnosis of cancer progression (133)(134)(135).…”

Section: Epithelial To Mesenchymal Transition Promotes Extracellular mentioning

confidence: 99%

Intrinsic and Extrinsic Modulators of the Epithelial to Mesenchymal Transition: Driving the Fate of Tumor Microenvironment

et al. 2020

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The epithelial to mesenchymal transition (EMT) is an evolutionarily conserved process. In cancer, EMT can activate biochemical changes in tumor cells that enable the destruction of the cellular polarity, leading to the acquisition of invasive capabilities. EMT regulation can be triggered by intrinsic and extrinsic signaling, allowing the tumor to adapt to the microenvironment demand in the different stages of tumor progression. In concomitance, tumor cells undergoing EMT actively interact with the surrounding tumor microenvironment (TME) constituted by cell components and extracellular matrix as well as cell secretome elements. As a result, the TME is in turn modulated by the EMT process toward an aggressive behavior. The current review presents the intrinsic and extrinsic modulators of EMT and their relationship with the TME, focusing on the non-cell-derived components, such as secreted metabolites, extracellular matrix, as well as extracellular vesicles. Moreover, we explore how these modulators can be suitable targets for anticancer therapy and personalized medicine.

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Actin cytoskeleton stiffness grades metastatic potential of ovarian carcinoma Hey A8 cells via nanoindentation mapping

Cited by 13 publications

References 36 publications

Biomechanics of Endothelial Tubule Formation Differentially Modulated by Cerebral Cavernous Malformation Proteins

Biomechanics of Endothelial Tubule Formation Differentially Modulated by Cerebral Cavernous Malformation Proteins

Examination of the relationship between viscoelastic properties and the invasion of ovarian cancer cells by atomic force microscopy

Intrinsic and Extrinsic Modulators of the Epithelial to Mesenchymal Transition: Driving the Fate of Tumor Microenvironment

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