<scp>MicroRNA</scp>‐204‐5p: A pivotal tumor suppressor

Yang, Fan; Bian, Zehua; Xu, Peiwen; Sun, Shengbai; Huang, Zijian

doi:10.1002/cam4.5077

Cited by 27 publications

(11 citation statements)

References 161 publications

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“…In contrast, miR-204/211 is expressed at detectable levels, which could be attributed to the low levels of TRPM-1/3, as TRPM3 was reported to be targeted by miR-204 ( Hall et al, 2014 ). miR-204 has been considered a tumor-suppressor microRNA, being negatively correlated with tumor malignancy ( Yang et al, 2023 ). In the colorectal cancer cell line HCT116, a highly invasive and metastatic cell line, PDIA1 levels were shown to be increased compared with normal or less aggressive colorectal cancer cell lines ( De Bessa et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Disturbed flow regulates protein disulfide isomerase A1 expression via microRNA-204

Tanaka,

Kumar,

Gutierre

et al. 2024

Front. Physiol.

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Redox processes can modulate vascular pathophysiology. The endoplasmic reticulum redox chaperone protein disulfide isomerase A1 (PDIA1) is overexpressed during vascular proliferative diseases, regulating thrombus formation, endoplasmic reticulum stress adaptation, and structural remodeling. However, both protective and deleterious vascular effects have been reported for PDIA1, depending on the cell type and underlying vascular condition. Further understanding of this question is hampered by the poorly studied mechanisms underlying PDIA1 expression regulation. Here, we showed that PDIA1 mRNA and protein levels were upregulated (average 5-fold) in the intima and media/adventitia following partial carotid ligation (PCL). Our search identified that miR-204-5p and miR-211-5p (miR-204/211), two broadly conserved miRNAs, share PDIA1 as a potential target. MiR-204/211 was downregulated in vascular layers following PCL. In isolated endothelial cells, gain-of-function experiments of miR-204 with miR mimic decreased PDIA1 mRNA while having negligible effects on markers of endothelial activation/stress response. Similar effects were observed in vascular smooth muscle cells (VSMCs). Furthermore, PDIA1 downregulation by miR-204 decreased levels of the VSMC contractile differentiation markers. In addition, PDIA1 overexpression prevented VSMC dedifferentiation by miR-204. Collectively, we report a new mechanism for PDIA1 regulation through miR-204 and identify its relevance in a model of vascular disease playing a role in VSMC differentiation. This mechanism may be regulated in distinct stages of atherosclerosis and provide a potential therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Disturbed flow regulates protein disulfide isomerase A1 expression via microRNA-204

Tanaka,

Kumar,

Gutierre

et al. 2024

Front. Physiol.

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“…In recent years an increasing number of studies on miRNAs as modulators of endothelial dysfunction have provided new insights into endothelial dysfunction, leading to potential new therapeutic approaches. miR-204-5p was reported to regulate apoptosis, autophagy, and cellular senescence by inhibiting target genes in multiple cell types [33][34][35] . Apoptosis is one of the most common phenotypes regulated by miR-204-5p and its target genes.…”

Section: Discussionmentioning

confidence: 99%

Salvianolic acid A alleviates H2O2-induced endothelial oxidative injury via miR-204-5p

Qiao,

Cao,

Chen

et al. 2024

Sci Rep

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Oxidative stress induced endothelial dysfunction plays a particularly important role in promoting the development of cardiovascular diseases (CVDs). Salvianolic acid A (SalA) is a water-soluble component of traditional Chinese medicine Salvia miltiorrhiza Bunge with anti-oxidant potency. This study aims to explore the regulatory effect of SalA on oxidative injury using an in vitro model of H2O2-induced injury in human umbilical vein endothelial cells (HUVECs). In the study, we determined cell viability, the activities of Lactate dehydrogenase (LDH) and Superoxide dismutase (SOD), cell proliferation rate and intracellular reactive oxygen species (ROS). Flow cytometry was used to detect cell apoptosis. Western-blotting was used to evaluate the expression of cell senescence, apoptosis, autophagy and pyroptosis protein factors. The expression level of miRNA was determined by qRT-PCR. Compared with H2O2-induced HUVECs, SalA promoted cell viability and cell proliferation rate; decreased LDH and ROS levels; and increased SOD activity. SalA also significantly attenuated endothelial senescence, inhibited cell apoptosis, reversed the increase of LC3 II/I ratio and NLRP3 accumulation. Furthermore, miR-204-5p was regulated by SalA. Importantly, miR-204-5p inhibitor had similar effect to that of SalA on H2O2-induced HUVECs. Our results indicated that SalA could alleviate H2O2-induced oxidative injury by downregulating miR-204-5p in HUVECs.

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“…In BC, the pathogenic role of miRNAs has been well-defined, and now it is well-assumed that several miRNAs are implicated in the tumor invasion and metastasis of BC cells [ 36 ]. Importantly, recent studies also determined that attenuation of microRNA-204-5p enhances the cell growth of human choriocarcinoma, suppresses apoptosis of cancerous cells, and plays a powerful role in pregnancy-induced hypertension [ 37 ]. Moreover, the role of hsa-miR-204-5p has also been demonstrated in atherosclerosis [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Gold Nanoparticles Inhibit PMA-Induced MMP-9 Expression via microRNA-204-5p Upregulation and Deactivation of NF-κBp65 in Breast Cancer Cells

Farhana

Alsrhani

Nazam

et al. 2023

Biology

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Objective: Breast cancer (BC) is the most common malignancy in females globally. Matrix metalloproteinase-9 (MMP-9) is crucial to the invasion, progression and spread of BC. Gold nanoparticles (AuNPs) have an anti-tumorigenic role, but their therapeutic role in microRNAs (miRNAs) regulation has not been explored. This study determined the potential of AuNPs against MMP-9 overexpression/production and miRNA-204-5p regulation in BC cells. Methods: AuNPs were newly engineered, and their stability was analyzed using the zeta potential, polydispersity index, surface-plasmon-resonance peak and transmission electron microscopy. A bioinformatics algorithm was used to predict the pairing of miRNA in the 3′untranslated-region (3′UTR) of MMP-9 mRNA. TaqMan assays were carried out to quantify miRNA and mRNA, whereas MMP-9-specific immunoassays and gelatin zymography were used to determine protein secretion and activity. The binding of miRNA in MMP-9 mRNA 3′UTR was verified by luciferase reporter clone assays and transfection with anti-miRNAs. In addition, NF-κBp65 activity was determined and confirmed with parthenolide treatment. Results: Engineered AuNPs were highly stable and spherical in shape, with a mean size of 28.3 nm. Tested in MCF-7 BC cells, microRNA-204-5p directly regulates MMP-9. AuNPs inhibit PMA-induced MMP-9 mRNA and protein via hsa-miR-204-5p upregulation. Anti-miR-204 transfected MCF-7 cells demonstrated enhanced MMP-9 expression (p < 0.001), while AuNPs treatment attenuated MMP-9 expression in a dose-dependent manner (p < 0.05). Moreover, AuNPs also inhibit PMA-induced NF-κBp65 activation in anti-hsa-miR-204 transfected MCF-7 cells. Conclusion: Engineered AuNPs were stable and non-toxic to BC cells. AuNPs inhibit PMA-induced MMP-9 expression, production and activation via NF-κBp65 deactivation and hsa-miR-204-5p upregulation. These novel therapeutic potentials of AuNPs on stimulated BC cells provide novel suggestions that AuNPs inhibit carcinogenic activity via inverse regulation of microRNAs.

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MicroRNA‐204‐5p: A pivotal tumor suppressor

Cited by 27 publications

References 161 publications

Disturbed flow regulates protein disulfide isomerase A1 expression via microRNA-204

Disturbed flow regulates protein disulfide isomerase A1 expression via microRNA-204

Salvianolic acid A alleviates H2O2-induced endothelial oxidative injury via miR-204-5p

Gold Nanoparticles Inhibit PMA-Induced MMP-9 Expression via microRNA-204-5p Upregulation and Deactivation of NF-κBp65 in Breast Cancer Cells

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