Syndecan-4 Promotes Epithelial Tumor Cells Spreading and Regulates the Turnover of PKCα Activity under Mechanical Stimulation on the Elastomeric Substrates

Huang, Chang-Wen; Cheng, Chao‐Min; Su, Hong-Lin; Lin, Yi‐Wen

doi:10.1159/000430297

Cited by 18 publications

(18 citation statements)

References 51 publications

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“…Cytokines and TGF-b cause fibroblasts within the matrix to modulate ECM, including aSMA expression [42]. aSMA expression is induced by TGF-b [43] Syndecan-4 is also necessary for transduction of signals through protein kinase C alpha (PKCa) activation resulting in the assembly of the actin cytoskeleton, cell contractility, and metastasis [44]. A Bleomycin model of fibrosis resulted in a 6-fold increased tissue stiffness compared to normal lung tissue.…”

Section: Fibroblastsmentioning

confidence: 99%

Precancerous niche (PCN), a product of fibrosis with remodeling by incessant chronic inflammation

Brücher

Jamall

2019

4open

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Fibroblasts are actively involved in the creation of the stroma and the extracellular matrix which are important for cell adhesion, cell–cell communication, and tissue metabolism. The role of fibrosis in carcinogenesis can be examined by analogy to tissues of various cancers. The orchestration of letters in the interplay of manifold components with signaling and crosstalk is incompletely understood but available evidence suggests a hitherto underappreciated role for fibrosis in carcinogenesis. Complex signaling and crosstalk by pathogenic stimuli evoke persistent subclinical inflammation, which in turn, results in a cascade of different cell types, ubiquitous proteins and their corresponding enzymes, cytokine releases, and multiple signaling pathways promoting the onset of fibrosis. There is considerable evidence that the body's attempt to resolve such a modified extracellular environment leads to further disruption of homeostasis and the genesis of the precancerous niche as part of the six-step process that describes carcinogenesis. The precancerous niche is formed and can be understood to develop as a result of (1) pathogenic stimulus, (2) chronic inflammation, and (3) fibrosis with alterations of the extracellular matrix, stromal rigidity, and mechano-transduction. This is why carcinogenesis is not just a process of aberrant cell growth with damaged genetic material but the role of the PCN in its entirety reveals how carcinogenesis can occur without invoking the need for somatic mutations.

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Section: Fibroblastsmentioning

confidence: 99%

Precancerous niche (PCN), a product of fibrosis with remodeling by incessant chronic inflammation

Brücher

Jamall

2019

4open

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“…The ECM microenvironment plays a crucial role in tumor cell progression. It provides a signal substrate and serves as an obstacle to the migrating cell body [9]. Cell migration involves a series of interdependent steps [5], of which the first step is the cell becoming polarized and elongating to form protrusions.…”

Section: Roles Of Myosins In Tumor Invasion and Metastasis Developmentmentioning

confidence: 99%

“…ROCK is implicated in inhibiting MLC phosphatase and elevating MLC phosphorylation and thus promoting cell contractility and adhesion [182]. Phosphorylated FAK can subsequently activate ERK1/2 and plays a similar role in the activation of MLC [9]. …”

Section: Myosin-mediated Factors Pathways and Models During Tumorigementioning

confidence: 99%

“…Such aspects include cell polarity loss [4], formation of protrusions [5], adhesion alteration [6], evasion of apoptosis [7], and cell invasion and movement [8]. Furthermore, the interactions between the developing tumor cells and the extracellular matrix microenvironment can also have significant impacts upon tumor progression [9]. The detection and the diagnostic and prognostic capabilities of molecular hallmarks in malignancies has recently become a primary focus of oncology research.…”

Section: Introductionmentioning

confidence: 99%

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Myosins as fundamental components during tumorigenesis: diverse and indispensable

Yang

2016

Oncotarget

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Myosin is a kind of actin-based motor protein. As the crucial functions of myosin during tumorigenesis have become increasingly apparent, the profile of myosin in the field of cancer research has also been growing. Eighteen distinct classes of myosins have been discovered in the past twenty years and constitute a diverse superfamily. Various myosins share similar structures. They all convert energy from ATP hydrolysis to exert mechanical stress upon interactions with microfilaments. Ongoing research is increasingly suggesting that at least seven kinds of myosins participate in the formation and development of cancer. Myosins play essential roles in cytokinesis failure, chromosomal and centrosomal amplification, multipolar spindle formation and DNA microsatellite instability. These are all prerequisites of tumor formation. Subsequently, myosins activate various processes of tumor invasion and metastasis development including cell migration, adhesion, protrusion formation, loss of cell polarity and suppression of apoptosis. In this review, we summarize the current understanding of the roles of myosins during tumorigenesis and discuss the factors and mechanisms which may regulate myosins in tumor progression. Furthermore, we put forward a completely new concept of “chromomyosin” to demonstrate the pivotal functions of myosins during karyokinesis and how this acts to optimize the functions of the members of the myosin superfamily.

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“…Cytoskeletal reorganization is a critical step in the process of tumor cell metastasis, which leads to the spread of cancer and to treatment failure [22,23,38]. Propofol has been found to influence the biological activity of several tumor cell lines by inducing cytoskeletal reorganization [26], but the processes driving the corresponding alterations in membrane ultrastructure have not been determined.…”

Section: Discussionmentioning

confidence: 99%

Effects of Propofol on Several Membrane Characteristics of Cervical Cancer Cell Lines

Zhang¹,

Wang²,

Cui³

et al. 2016

Cell Physiol Biochem

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Background: Although significant advances have been made toward understanding the molecular mechanisms underlying the effect of propofol on tumor cell metastasis, less is known regarding how cell membrane and cytoskeletal ultrastructure are affected in this process. Here, we investigated the relationship between cell morphology and cell size, which are features mainly defined by the cytoskeleton. Methods: To confirm the effects of propofol on the migratory ability of human cervical carcinoma cells, cell migration and invasion were examined through scratch wound healing and transwell membrane assays. Furthermore, HeLa cells cultivated with different concentrations of propofol were examined by confocal microscopy and atomic force microscopy (AFM), and the mean optical density and migration ability of these cells were also assessed. In addition, cell membrane morphology was inspected using AFM. Results:The results of the wound healing and transwell membrane assays indicated that propofol decreases the migratory ability of cervical carcinoma cells compared to control cells. A comparative analysis of the test results revealed that short-term (3 h) exposure to propofol induced marked changes in cell membrane microstructure and in the cytoskeleton in a dose-dependent manner. These morphological changes in the cell membrane were accompanied by cytoskeleton (F-actin) derangement. The present findings demonstrate a close relationship between changes in cell membrane ultrastructure and cytoskeletal alterations (F-actin) in propofol-treated HeLa cells. AFM scanning analysis showed that cell membrane ultrastructure was significantly changed, including a clear reduction in membrane roughness. Conclusion:The influence of propofol on the HeLa cell cytoskeleton can be directly reflected by changes in cellular morphology, as assessed by AFM. Moreover, the use of AFM is a good method for investigating propofol-mediated changes within cytoskeletal ultrastructure.

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Syndecan-4 Promotes Epithelial Tumor Cells Spreading and Regulates the Turnover of PKCα Activity under Mechanical Stimulation on the Elastomeric Substrates

Cited by 18 publications

References 51 publications

Precancerous niche (PCN), a product of fibrosis with remodeling by incessant chronic inflammation

Precancerous niche (PCN), a product of fibrosis with remodeling by incessant chronic inflammation

Myosins as fundamental components during tumorigenesis: diverse and indispensable

Effects of Propofol on Several Membrane Characteristics of Cervical Cancer Cell Lines

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