Cell adhesion century: culture breakthrough

Kendall, Kevin

doi:10.1098/rstb.2014.0025

Cited by 1 publication

(1 citation statement)

References 17 publications

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“…E-cadherin (E-cad), the product of the E-cadherin gene ( CDH1 ) located on the long arm of chromosome 16 (16q22.1), is a calcium-dependent epithelial transmembrane glycoprotein that mediates cell-to-cell adhesion and helps maintain the morphological integrity of epithelial cells by forming homodimers with E-cadherin molecules on adjacent cells via its extracellular domain 16. N-cadherin (N-cad) is a 140 kDa protein and is an integral membrane, calcium-binding glycoprotein that mediates the intercellular adhesion 17,18. Presence of N-cadherin is associated with more aggressive behavior of epithelial-derived solid malignancies and can be regarded as a predictor of poor survival, based on meta-analysis involving 36 studies with 5705 patients 19.…”

Section: Introductionmentioning

confidence: 99%

<p>Histone deacetylase inhibitors reinforce the phenotypical markers of breast epithelial or mesenchymal cancer cells but inhibit their migratory properties</p>

Wawruszak¹,

Gumbarewicz²,

Okon³

et al. 2019

CMAR

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IntroductionHistone deacetylase inhibitors (HDIs) are a group of compounds that exhibit anticancer activity, but their significance and usefulness in breast cancer (BC) treatment are still controversial. The ability of cancer cells to invade and migrate is augmented by the acquisition of a mesenchymal phenotype – a process known as epithelial-to-mesenchymal transition (EMT). Changes in the expression level of different cadherins, so-called cadherin switches, have been used to monitor the EMT process in development and tumor progression, in particular migration and invasion potential. The aim of this study was to analyze the influence of two HDIs – valproic acid (VPA) and vorinostat (SAHA) – on the migration potential of different BC cell types, as well as on EMT, or its reverse process – mesenchymal-to-epithelial transition, progression by means of shift in epithelial and mesenchymal marker expression.MethodsHDI treatment-induced expression of E- and N-cadherin at the mRNA and protein levels was evaluated by qPCR, Western blotting and immunostaining methods, respectively. BC cell proliferation and migration were assessed by BrdU, xCELLigence system and wound-healing assay.ResultsVPA and SAHA inhibited the proliferation and migration in a dose- and time-dependent manner, regardless of the BC cell type. Unawares, BC cells having a more mesenchymal phenotype (MDA-MB-468) were found to overexpress N-cadherin, whereas BC lines having an epithelial phenotype (T47D, MCF7) responded to HDI treatment by a significant increase of E-cadherin expression.DiscussionWe suggest that HDAC inhibition results in a more relaxed chromatin concomitant to an increase in the expression of already expressing genes.ConclusionBy using multiple cancer cell lines, we conclude that HDI induction or reversal of EMT is not a universal mechanism, yet inhibition of cell migration is, and thus EMT should not be considered as the only measurement for tumor aggressiveness.

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