<scp>MiR</scp>‐122‐5p and <scp>miR</scp>‐326‐3p promote cadmium‐induced <scp>NRK‐52E</scp> cell apoptosis by downregulating <scp>PLD1</scp>

Wang, Yuan; Liang, Lixia; Deng, Yaotang; Dong, Ming; Wang, Guanghai; Zou, Fei

doi:10.1002/tox.22998

Cited by 22 publications

(17 citation statements)

References 30 publications

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“…Aberrant apoptosis, a typical characteristic in the epithelial layer of OLP, impairs the integrity of oral epithelia barrier against bacteria 28,29 . In this study, we verified that miR‐122 overexpression leads to excess cell apoptosis in HOKs, which is in accordant with previous observations indicate that miR‐122 regulates apoptosis in various cell types and diseases 26,27 . In addition, consistent with early reports, 24 substantial TUNEL‐stained oral keratinocytes were observed in the specimens from OLP patients.…”

Section: Discussionsupporting

confidence: 92%

“…Up‐regulation of miR‐122 induces cell apoptosis in oral keratinocytes. MiR‐122 is able to regulate cell apoptosis in a variety of cell types 26,27 . To better understand the role of miR‐122 in apoptosis of oral keratinocytes, we treated HOKs with miR‐122 mimics.…”

Section: Resultsmentioning

confidence: 99%

“…Both miR‐122 and VDR are associated with cell apoptosis in several cell types 24,26,27 . Apoptosis is regarded as a characteristic of OLP leading to the excessive loss of oral keratinocytes 24,28 .…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‐122 promotes apoptosis of keratinocytes in oral lichen planus through suppressing VDR expression

Xie

Wang

et al. 2021

J Cellular Molecular Medi

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Oral lichen planus (OLP), a common immune-mediated disease, shows oral ulceration and persistent inflammation in patients those who experience discomfort and remarkable impairments of oral functioning and life quality. 1 Albeit OLP is regarded as an inflammatory disorder, malignant transformation rate of OLP is approximately 1.4% within 7 years. 2 Ulceration, gender and location on the tongue are key risky factors responsible for malignant transformation. 2 There are six subtypes of OLP in clinic, including atrophic, reticular,

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Section: Discussionsupporting

confidence: 92%

Section: Resultsmentioning

confidence: 99%

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MicroRNA‐122 promotes apoptosis of keratinocytes in oral lichen planus through suppressing VDR expression

Xie

Wang

et al. 2021

J Cellular Molecular Medi

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“…Cadmium (Cd), a toxic heavy metal, could be accumulated in human bodies through drinking water, foods, occupational exposure, and so on 1 . Previous reports have demonstrated that Cd could induce oxidative stress, DNA damage, apoptosis, and mitophagy 2–4 . More importantly, a vast majority of studies have reported that Cd could promote cell proliferation in many cancer cells 5 .…”

Section: Introductionmentioning

confidence: 99%

Low‐dose cadmium exposure facilitates cell proliferation by promoter hypermethylation of RASSF1A and DAPK1 genes

Zhang

Tang

et al. 2021

Environmental Toxicology

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Cadmium (Cd) at low concentrations has a potential to promote cell proliferation. However, the molecular mechanisms of Cd‐induced proliferation are not well understood. Here, we reported that Cd (0–500 nM) significantly promoted the proliferation of HepG2 cells as demonstrated by elevated cell viability, more EdU‐positive cells and increased gene expression of KI‐67 and COX‐2. Meanwhile, the gene expression of DNA methyltransferases was found to be elevated while that of tumor suppressor genes DAPK1 and RASSF1A were decreased under Cd exposure. Correspondingly, the methylation level of promoters in DAPK1 and RASSF1A were increased. Specifically, the CpG sites at −461 (Chr3:50, 374, 481) of RASSF1A promoter, and that at −260 (Chr9:90, 113, 207), −239 (Chr9:90, 113, 228), and −68 (Chr9:90, 113, 399) of DAPK1 promoter, were significantly hypermethylated. Moreover, 5‐azacytidine (an inhibitor of DNA methyltransferase) partly impaired Cd‐induced promoter hypermethylation of RASSF1A and DAPK1 genes, increased their expressions and slowed down Cd‐induced cell proliferation, suggesting that DNA methylation play an essential part in Cd‐boosted proliferation. The study showed that Cd caused promoter hypermethylation of RASSF1A and DAPK1, decreasing their expression and leading to higher level of cell proliferation. Furthermore, Cd at low concentrations could influence DNA methylation, which may serve as the proliferative mechanism of Cd.

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“… 26 In addition, miR‐326‐3p enhances cadmium‐triggered NRK‐52E cell apoptosis via down‐regulating PLD1. 27 Here, miR‑326‐3p was down‐regulated in VSMCs treated with ox‐LDL and it was negatively modulated by circ_0002984. Next, overexpression of miR‑326‐3p reversed the circ_0002984 overexpressing‑induced effects on the viability, migration and inflammation of VSMCs.…”

Section: Discussionmentioning

confidence: 85%

Circ_0002984 induces proliferation, migration and inflammation response of VSMCs induced by ox‐LDL through miR‑326‐3p/VAMP3 axis in atherosclerosis

Jiang

Zheng

2021

J Cellular Molecular Medi

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Atherosclerosis can result in multiple cardiovascular diseases. Circular RNAs (CircRNAs) have been reported as significant non‐coding RNAs in atherosclerosis progression. Dysfunction of vascular smooth muscle cells (VSMCs) is involved in atherosclerosis. However, up to now, the effect of circ_0002984 in atherosclerosis is still unknown. Currently, we aimed to investigate the function of circ_0002984 in VSMCs incubated by oxidized low‐density lipoprotein (ox‐LDL). Firstly, our findings indicated that the expression levels of circ_0002984 were significantly up‐regulated in the serum of atherosclerosis patients and ox‐LDL‐incubated VSMCs. Loss of circ_0002984 suppressed VSMC viability, cell cycle distribution and migration capacity. Then, we carried out ELISA assay to determine TNF‐α and IL‐6 levels. The data implied that lack of circ_0002984 obviously repressed ox‐LDL–stimulated VSMC inflammation. Meanwhile, miR‐326‐3p, which was predicted as a target of circ_0002984, was obviously down‐regulated in VSMCs treated by ox‐LDL. Additionally, after overexpression circ_0002984 in VSMCs, a decrease in miR‐326‐3p was observed. Subsequently, miR‐326‐3p was demonstrated to target vesicle‐associated membrane protein 3 (VAMP3). Therefore, we hypothesized that circ_0002984 could modulate expression of VAMP3 through sponging miR‐326‐3p. Furthermore, we confirmed that up‐regulation of miR‐326‐3p rescued the circ_0002984 overexpressing‐mediated effects on VMSC viability, migration and inflammation. Additionally, miR‐326‐3p inhibitor‐mediated functions on VSMCs were reversed by knockdown of VAMP3. In conclusion, circ_0002984 mediated cell proliferation, migration and inflammation through modulating miR‐326‐3p and VAMP3 in VSMCs, which suggested that circ_0002984 might hold great promise as a therapeutic strategy for atherosclerosis.

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MiR‐122‐5p and miR‐326‐3p promote cadmium‐induced NRK‐52E cell apoptosis by downregulating PLD1

Cited by 22 publications

References 30 publications

MicroRNA‐122 promotes apoptosis of keratinocytes in oral lichen planus through suppressing VDR expression

MicroRNA‐122 promotes apoptosis of keratinocytes in oral lichen planus through suppressing VDR expression

Low‐dose cadmium exposure facilitates cell proliferation by promoter hypermethylation of RASSF1A and DAPK1 genes

Circ_0002984 induces proliferation, migration and inflammation response of VSMCs induced by ox‐LDL through miR‑326‐3p/VAMP3 axis in atherosclerosis

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