Distribution of c-myc oncoprotein in healthy and atherosclerotic human carotid arteries

Marin, Michael L.; Gordon, Ronald E.; Veith, Frank J.; Tulchin, Natalie; Panetta, Thomas F.

doi:10.1016/0741-5214(93)90596-e

Cited by 25 publications

(7 citation statements)

References 25 publications

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“…The data presented in the present study indicated that the expression levels of Bcl-2 and c-myc were significantly increased in the blood cells from patients with atherosclerosis compared with the healthy controls. Consistent with these results, a previous study revealed that c-myc was overexpressed in plaque SMCs (44). However, a small number of studies contradict the Bcl-2 data from the present study (45,46).…”

Section: Discussionsupporting

confidence: 90%

CircRNA‑0044073 is upregulated in atherosclerosis and increases the proliferation and invasion of cells by targeting miR‑107

Shen

Lou

et al. 2019

Mol Med Report

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Circular RNAs (circRNAs) are endogenous non-coding RNAs implicated in atherosclerosis. The aim of the present study was to explore the function of circRNA-0044073 in atherosclerosis. Reverse transcription quantitative polymerase chain reaction assays were used to measure the expression levels of circRNA-0044073, microRNA (miRNA/miR)-107, janus kinase 1 (JAK1), signal transducer and activator of transcription 3 (STAT3), B-cell lymphoma 2 (Bcl-2) and v-myc avian myelocytomatosis viral oncogene homolog (c-myc) in in blood cells from patients with atherosclerosis. RNA pull-down and luciferase reporter assays were then used to determine the association between circRNA and miR expression, and miR and gene expression, respectively. Matrigel invasion assay and flow cytometry were used to analyze cell invasion and cell cycle. Western blot analysis and ELISA were used to evaluate the expression levels of proteins. It was identified that the expression of circRNA-0044073 was upregulated and the expression of miR-107 was downregulated in atherosclerotic blood cells. Overexpression of circRNA-0044073 promoted the proliferation of human vascular smooth muscle cells (HUVSMCs) and human vascular endothelial cells (HUVECs), while overexpression of miR-107 inhibited their proliferation. In addition, circRNA-0044073 suppressed the levels of miR-107 via a sponge mechanism. Lipopolysaccharide (LPS) affected the proliferation of HUVSMCs and HUVECs, and also resulted in changes in circRNA-0044073 expression levels. CircRNA-0044073 promoted the proliferation and invasion of HUVSMCs and HUVECs in spite of the opposite effect observed with LPS treatment. The JAK/STAT signaling pathway was activated in patients with atherosclerosis. CircRNA-0044073 favored the activation of the JAK/STAT signaling pathway and inflammation in HUVSMCs and HUVECs. These data indicate that circRNA-0044073 is upregulated in atherosclerosis and promotes the proliferation and invasion of cells by targeting miR-107 and activating the JAK/STAT signaling pathway, potentially offering a target for novel treatment strategies against atherosclerosis.

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Section: Discussionsupporting

confidence: 90%

CircRNA‑0044073 is upregulated in atherosclerosis and increases the proliferation and invasion of cells by targeting miR‑107

Shen

Lou

et al. 2019

Mol Med Report

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“…10,11 Furthermore, it has been reported that overexpression of PDGF, c-myc and other protooncogenes occurs in atherosclerotic vascular lesions. [11][12][13] The monoclonal hypothesis is also consistent with the observations that carcinogenic agents, like chemical mutagens, radiations and oncogenic viruses, can induce atherosclerotic lesions in laboratory animals and have atherogenic effects in human population. 2,[14][15][16][17][18][19] Certainly, the "response to injury" and the "monoclonal" theories of atherosclerosis are not mutually exclusive and can be unified as described in Figure 2.…”

Section: The Development Of Atherosclerosissupporting

confidence: 68%

Genetic Instability, DNA Damage and Atherosclerosis

Andreassi¹,

Botto²

2003

Cell Cycle

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“…The oxidation-sensitive c-myc-dependent signaling events are attenuated by intervention with antioxidants like vitamin E (5), which may also reduce atherogenesis in experimental models (6). Indeed, enhanced c-Myc expression was described in human cells such as VSMC from aortic plaques (7) or carotid atherosclerotic lesions (8), in vein graft VSMC hyperplasia (9), and in human coronary cells incubated with oxidized low density lipoprotein (LDL), as well as in early coronary lesions of WHHL rabbits (5). However, it is yet unclear whether activation of c-Myc in the vascular wall during chronic hypercholesterolemia precedes development of overt atherosclerotic lesions.…”

mentioning

confidence: 98%