The Role of Immunoglobulin Superfamily Cell Adhesion Molecules in Cancer Metastasis

Wong, Chee Wai; Dye, Danielle E.; Coombe, Deirdre R.

doi:10.1155/2012/340296

Cited by 140 publications

(84 citation statements)

References 92 publications

(124 reference statements)

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“…Subsequently, other cell–cell adhesion families emerged, including: lectin cell adhesion molecules (LEC-CAMs; for example selectins), which mediate lymphocyte homing and leukocyte–endothelial interactions 49,50 ; and IgSF-CAMs, which mediate various cell–cell interactions 51 . IgSF-CAMs include intercellular adhesion molecule 1 (ICAM1) and vascular cell adhesion protein (VCAM), which are also involved in leukocyte–endothelial interactions, as well as NCAM.…”

Section: Cell–cell Adhesion Moleculesmentioning

confidence: 99%

The origins of the molecular era of adhesion research

Horwitz¹

2012

Nat Rev Mol Cell Biol

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Recognition of the importance of cell adhesion grew steadily during the twentieth century as it promised answers to fundamental questions in diverse fields that included cell biology, developmental biology, tumorigenesis, immunology and neurobiology. However, the route towards a better understanding of its molecular basis was long and difficult, with many false starts. Major progress was made in the late 1970s to late 1980s with the identification of the major families of adhesion molecules, including integrins and cadherins. This in turn set the stage for the explosive growth in adhesion research over the past 25 years.

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Section: Cell–cell Adhesion Moleculesmentioning

confidence: 99%

The origins of the molecular era of adhesion research

Horwitz¹

2012

Nat Rev Mol Cell Biol

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“…Besides mediating cell adhesion, there is increasing evidence that CAMs also function as receptors which modulate signal transduction in many cellular processes including proliferation, apoptosis, migration and differentiation. Deregulation of these biological processes in malignant tumors has been associated with the aberrant expression of CAMs, demonstrating that alterations in CAMs play a pivotal role in cancer development and progression12.…”

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confidence: 99%

HepaCAM associates with connexin 43 and enhances its localization in cellular junctions

Moh

Schwarz

2016

Sci Rep

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HepaCAM (GlialCAM) is frequently deleted in carcinomas, and reintroduction of hepaCAM into transformed cell lines reduces cellular growth and induces senescence. Mutations in HEPACAM give rise to the neurodegenerative disease megalencephalic leukoencephalopathy with subcortical cysts (MLC) since mutated hepaCAM prevents shuttling of MLC1 protein to astrocytic junctions in the plasma membrane. Here we identify that hepaCAM associates with connexin 43, a main component of gap junctions, and enhances connexin 43 localization to the plasma membrane at cellular junctions. HepaCAM also increases the levels of connexin 43, not by enhancing its transcription but by stabilizing connexin 43 protein. In the absence of hepaCAM, connexin 43 undergoes a faster degradation via the lysosomal pathway while proteasomal degradation seems not to be involved. Mutations in hepaCAM that cause MLC, or neutralization of hepaCAM by antibodies disrupt its association with connexin 43 at cellular junctions. By discovering the requirement of hepaCAM for localizing connexin 43, a well-established tumor suppressor, to cellular junctions and stabilizing it there, this study suggests a mechanism by which deletion of hepaCAM may support tumor progression.

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“…Endoglin, a membrane glycoprotein located on cell surfaces being part of the TGF -β receptor complex, is involved in the cytoskeleton organization and affects cell morphology and migration 26 ; its expression was again decreased substantially (a ratio of 0.62 for treated/untreated cells). L1CAM and NEO1, which belong to the immunoglobulin super-family and play important roles in cell-cell adhesion 27, 28 , were down-regulated to levels that are 65% and 28% of those of control cells, respectively.…”

Section: Resultsmentioning

confidence: 95%

Quantitative Proteomic Analysis Revealed N′-Nitrosonornicotine-induced Down-regulation of Nonmuscle Myosin II and Reduced Cell Migration in Cultured Human Skin Fibroblast Cells

Prins

Wang

2013

J. Proteome Res.

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The association of tobacco smoke with decreased cell motility and wound healing is well documented; however, the cellular mechanisms and specific toxic tobacco constituents responsible for this effect are not well understood. Tobacco-specific N-nitrosamines (TSNAs) are among the most important classes of carcinogens found in tobacco products. The TSNA N′-nitrosonornicotine (NNN) is present at relatively high levels in tobacco and its smoke, as well as second- and third-hand smoke. To investigate the cellular pathways that are perturbed upon NNN exposure, we employed a quantitative proteomic approach, utilizing stable isotope labeling by amino acids in cell culture and mass spectrometry, to assess the NNN-induced alteration of protein expression in GM00637 human skin fibroblast cells. With this approach, we were able to quantify 2599 proteins, 191 of which displayed significantly changed expression following NNN exposure. One of the main findings from our proteomic analysis was the down-regulation of six different subunits of myosin, particularly non-muscle myosin II heavy chain, isoforms A, B, and C. In addition, we found the altered expression of several extracellular matrix proteins and proteins involved in cellular adhesion. Together, our quantitative proteomic results suggested that NNN exposure may interfere with fibroblast motility. An in vitro scratch wound assay results supported that NNN exposure reduced the ability of dermal fibroblast to migrate into the scratched area. The results from the present study offered novel insights into the cellular mechanisms of NNN toxicity and identified NNN as a specific tobacco constituent that contributes to decreased fibroblast migration.

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The Role of Immunoglobulin Superfamily Cell Adhesion Molecules in Cancer Metastasis

Cited by 140 publications

References 92 publications

The origins of the molecular era of adhesion research

The origins of the molecular era of adhesion research

HepaCAM associates with connexin 43 and enhances its localization in cellular junctions

Quantitative Proteomic Analysis Revealed N′-Nitrosonornicotine-induced Down-regulation of Nonmuscle Myosin II and Reduced Cell Migration in Cultured Human Skin Fibroblast Cells

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