Biological aspects of signal transduction by cell adhesion receptors

Reddig, Peter J.; Juliano, Rudolph L.

doi:10.1016/s0074-7696(02)20005-4

Cited by 83 publications

(64 citation statements)

References 209 publications

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“…Cross-signaling between cadherins and other adhesion molecules is a common phenomenon [1]. Ep-CAM expression is associated with proliferation and inhibits epithelial differentiation [7,9,12].…”

Section: Discussionmentioning

confidence: 99%

“…Responding to external signals requires many secondary pathways within the cells in order to respond accurately and in a coordinated fashion [1]. Disturbances in these pathways could lead to dramatic dysfunctioning of the cell, for example carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

“…It participates in various regulating mechanisms, for example in cytoplasmic-to nuclear signaling, vesicle transport, cytoskeletal rearrangements and CD28-B7 outside-inside signaling [1,4,5]. Important target molecules are the small Rho GTPases, which are involved in cytoskeletal organization.…”

Section: Introductionmentioning

confidence: 99%

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Cadherins are regulated by Ep-CAM via phosphaditylinositol-3 kinase

et al. 2007

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cadherins are regulated by Ep-CAM via phosphaditylinositol-3 kinase

et al. 2007

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“…This initiates a downstream proteolytic cascade affecting signalling molecules like focal adhesion-kinase (FAK), Cas and paxillin [6,[41][42][43]. Cleavage of FAK shuts down its survival signal and disrupts focal adhesion architecture [44]. p130Cas cleavage produces a carboxy-terminal fragment, which regulates transcription of p21 cyclin kinase inhibitor, thus contributing to anoikis execution by blocking the cell cycle [45].…”

Section: Extrinsic Pathwaymentioning

confidence: 99%

“…The role of ECM as anoikis suppressor is well established [1,49] and several integrins (α1β1, α2β1, α3β1, α5β1, α6β1, α6β4, αvβ3) have a profound impact on cell survival [2,44,50] in both normal or neoplastic cells [2,51,52]. Key players in integrin-mediated signal transduction leading to anoikis protection are FAK, integrin-linked kinase (ILK), Src tyrosine kinase, PI3K, ERK and the adaptor protein Shc (Figure 2).…”

Section: Physiological Protection From Anoikismentioning

confidence: 99%

Anoikis: an emerging hallmark in health and diseases

Taddei

Giannoni

Fiaschi

et al. 2011

The Journal of Pathology

528

404

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Anoikis is a programmed cell death occurring upon cell detachment from the correct extracellular matrix, thus disrupting integrin ligation. It is a critical mechanism in preventing dysplastic cell growth or attachment to an inappropriate matrix. Anoikis prevents detached epithelial cells from colonizing elsewhere and is thus essential for tissue homeostasis and development. As anchorage-independent growth and epithelial-mesenchymal transition, two features associated with anoikis resistance, are crucial steps during tumour progression and metastatic spreading of cancer cells, anoikis deregulation has now evoked particular attention from the scientific community. The aim of this review is to analyse the molecular mechanisms governing both anoikis and anoikis resistance, focusing on their regulation in physiological processes, as well as in several diseases, including metastatic cancers, cardiovascular diseases and diabetes.

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A Circulating Bioreactor Reprograms Cancer Cells Toward a More Mesenchymal Niche

et al. 2020

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Cancer is a complex and heterogeneous disease, and cancer cells dynamically interact with the mechanical microenvironment such as hydrostatic pressure, fluid shear, and interstitial flow. These factors play an essential role in cell fate and circulating tumor cell heterogeneity, and can influence the cellular phenotype. In this study, a peristaltic continuous flow reactor is designed and applied to HCT‐116 colorectal carcinoma cells to mimic the fluid dynamics of circulation. With this intervention, a CD44/CD24‐cell subpopulation emerges, and 100 genes are significantly regulated. The expression of cells at 4 h in the flow reactor is very similar to TGF‐ß treatment, which is an inducer of epithelial–mesenchymal transition. ATF3 and SERPINE1 are significantly upregulated in these groups, suggesting that the mesenchymal transition is induced through this signaling pathway. This flow reactor model is satisfactory on its own to reprogram colorectal cancer cells toward a more mesenchymal niche mimicking circulation of the blood.

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Biological aspects of signal transduction by cell adhesion receptors

Cited by 83 publications

References 209 publications

Cadherins are regulated by Ep-CAM via phosphaditylinositol-3 kinase

Cadherins are regulated by Ep-CAM via phosphaditylinositol-3 kinase

Anoikis: an emerging hallmark in health and diseases

A Circulating Bioreactor Reprograms Cancer Cells Toward a More Mesenchymal Niche

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