CD146 (Cluster of Differentiation 146)

Leroyer, Aurélie S.; Blin, Muriel G.; Bachelier, Richard; Bardin, Nathalie; Blot‐Chabaud, Marcel; Dignat-George, Françoise

doi:10.1161/atvbaha.119.312653

Cited by 59 publications

(62 citation statements)

References 76 publications

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“…Similarly, MCF-10F cells treated with parathion or malathion, alone or combined with estrogen, induced changes in cell adhesion molecules such as CD146 (35), a surface protein also known as melanoma cell adhesion molecule (200) that is involved in cell adhesion and other processes, including cell proliferation, migration and progression, and particularly angiogenesis and vascular permeability (201)(202)(203)(204). The aforementioned treatments also upregulated keratin 18 expression; another component of epithelial cells that protects them from external forces, serves as a biomarker in epithelial cancers and plays other roles in drug response and tumorigenesis (205)(206)(207)(208)(209)(210)(211)(212)(213)(214)(215).…”

Section: Parathion and Malathion Cause Genomic Instabilitymentioning

confidence: 99%

Signs of carcinogenicity induced by parathion, malathion, and estrogen in human breast epithelial cells (Review)

2021

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Cancer development is a multistep process that may be induced by a variety of compounds. Environmental substances, such as pesticides, have been associated with different human diseases. Organophosphorus pesticides (OPs) are among the most commonly used insecticides. Despite the fact that organophosphorus has been associated with an increased risk of cancer, particularly hormone-mediated cancer, few prospective studies have examined the use of individual insecticides. Reported results have demonstrated that OPs and estrogen induce a cascade of events indicative of the transformation of human breast epithelial cells. In vitro studies analyzing an immortalized non-tumorigenic human breast epithelial cell line may provide us with an approach to analyzing cell transformation under the effects of OPs in the presence of estrogen. The results suggested hormone-mediated effects of these insecticides on the risk of cancer among women. It can be concluded that, through experimental models, the initiation of cancer can be studied by analyzing the steps that transform normal breast cells to malignant ones through certain substances, such as pesticides and estrogen. Such substances cause genomic instability, and therefore tumor formation in the animal, and signs of carcinogenesis in vitro. Cancer initiation has been associated with an increase in genomic instability, indicated by the inactivation of tumor-suppressor genes and activation of oncogenes in the presence of malathion, parathion, and estrogen. In the present study, a comprehensive summary of the impact of OPs in human and rat breast cancer, specifically their effects on the cell cycle, signaling pathways linked to epidermal growth factor, drug metabolism, and genomic instability in an MCF-10F estrogen receptor-negative breast cell line is provided.

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Section: Parathion and Malathion Cause Genomic Instabilitymentioning

confidence: 99%

Signs of carcinogenicity induced by parathion, malathion, and estrogen in human breast epithelial cells (Review)

2021

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Section: Cd146mentioning

confidence: 99%

“…CD146 has been recently proposed as a potential therapeutic target based on its involvement in vascular integrity [158]. Three forms of CD146 have been described and include two transmembrane isoforms, long CD146 (lgCD146) and short CD146 (shCD146), as well as a soluble isoform (sCD146), which circulates in the plasma and derives from metalloprotease-dependent shedding of the previous two proteins [158]. The lgCD146 and shCD146 isoforms are, respectively, generated by either inclusion or skipping of exon 15 and characterized by different intracellular domains, as well as by diverse cellular localization [158].…”

Section: Cd146mentioning

confidence: 99%

Alternative splicing in endothelial cells: novel therapeutic opportunities in cancer angiogenesis

Matteo

Belloni

Pradella

et al. 2020

J Exp Clin Cancer Res

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Alternative splicing (AS) is a pervasive molecular process generating multiple protein isoforms, from a single gene. It plays fundamental roles during development, differentiation and maintenance of tissue homeostasis, while aberrant AS is considered a hallmark of multiple diseases, including cancer. Cancer-restricted AS isoforms represent either predictive biomarkers for diagnosis/prognosis or targets for anti-cancer therapies. Here, we discuss the contribution of AS regulation in cancer angiogenesis, a complex process supporting disease development and progression. We consider AS programs acting in a specific and non-redundant manner to influence morphological and functional changes involved in cancer angiogenesis. In particular, we describe relevant AS variants or splicing regulators controlling either secreted or membrane-bound angiogenic factors, which may represent attractive targets for therapeutic interventions in human cancer.

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“…The molecular mechanisms associated with this receptor are angiogenesis, vessel permeability and leukocyte transendothelial migration. 46 CD146 has been described as a pro-angiogenic mediator, counterbalancing the UNC5b anti-angiogenic signal. Further studies are needed to clarify which signalling pathways it utilises in leukocytes to modulate their migration.…”

Section: Netrin-1 Receptorsmentioning

confidence: 99%

Netrin-1: Focus on its role in cardiovascular physiology and atherosclerosis

Claro

Ferro

2020

JRSM Cardiovascular Disease

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The netrins form a family of laminin-related proteins which were first described as modulators of cell migration and axonal guidance during fetal development. Netrin-1 is the most extensively studied member of this family and, since its discovery, non-neural roles have been associated with it. Together with its receptors, DCC/neogenin and UNC5, netrin-1 has been shown to be involved in the regulation of angiogenesis, organogenesis, cancer and inflammation. An NF-κB-dependent truncated isoform of netrin-1 has also been shown to be produced in endothelial and some types of cancer cells, which both accumulates in and affects the function of the nucleus. In atherosclerosis, conflicting roles for netrin-1 have been reported on plaque progression via its receptor UNC5b. Whereas endothelial-derived netrin-1 inhibits chemotaxis of leukocytes and reduces the migration of monocytes to the atherosclerotic plaque, netrin-1 expressed by macrophages within the plaque plays a pro-atherogenic role, promoting cell survival, recruiting smooth muscle cells and inhibiting foam cell egress to the lymphatic system. In contrast, there is evidence that netrin-1 promotes macrophage differentiation to an alternative activated phenotype and induces expression of IL-4 and IL-13, while downregulate expression of IL-6 and COX-2. Further work is needed to elucidate the precise roles of the two isoforms of netrin-1 in different cell types in the context of atherosclerosis, and its potential as a putative novel therapeutic target in this disease.

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CD146 (Cluster of Differentiation 146)

Cited by 59 publications

References 76 publications

Signs of carcinogenicity induced by parathion, malathion, and estrogen in human breast epithelial cells (Review)

Signs of carcinogenicity induced by parathion, malathion, and estrogen in human breast epithelial cells (Review)

Alternative splicing in endothelial cells: novel therapeutic opportunities in cancer angiogenesis

Netrin-1: Focus on its role in cardiovascular physiology and atherosclerosis

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