MiR‐182‐5p inhibited oxidative stress and apoptosis triggered by oxidized low‐density lipoprotein via targeting toll‐like receptor 4

Qin, Song-Bai; Peng, Da-Yan; Lu, Jing‐Min; Ke, Zun‐Ping

doi:10.1002/jcp.26389

Cited by 64 publications

(51 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As we known, miRNAs regulate lives' activities by means of the protein indirect role and regulate target genes by binding to the 3'UTR of specific mRNAs and cause degradation or transcriptional inhibition of target genes [31][32][33][34][35][36]. Biological softwares were used to predict the possible target genes of miR-182-5p to investigate the mechanisms of these miRNAs in renal cancer.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

Wang

et al. 2020

Mol Cancer

101

View full text Add to dashboard Cite

Background: Accumulating literatures have indicated that long non-coding RNAs (lncRNAs) are potential biomarkers that play key roles in tumor development and progression. Urothelial cancer associated 1 (UCA1) is a novel lncRNA that acts as a potential biomarker and is involved in the development of cancers. However, the molecular mechanism of UCA1 in renal cancer is still needed to further explore. Methods: The relative expression level of UCA1 was determined by Real-Time qPCR in a total of 88 patients with urothelial renal cancer and in different renal cancer cell lines. Loss-of-function experiments were performed to investigate the biological roles of UCA1 and miR-182-5p on renal cancer cell proliferation, migration, apoptosis and tumorigenicity. Comprehensive transcriptional analysis, dual-luciferase reporter assay and western blot etc. were performed to explore the molecular mechanisms underlying the functions of UCA1. Results: In this study, we found that UCA1 was significantly up-regulated in renal cancer. Moreover, increased UCA1 expression was positively correlated with differentiation and advanced TNM stage. Further experiments demonstrated that knockdown of UCA1 inhibited malignant phenotypes and Notch signal path of renal cancer cells, and miR-182-5p was reverse function as UCA1. UCA1 functioned as a miRNA sponge to positively regulate the expression of Delta-like ligand 4(DLL4) through sponging miR-182-5p and subsequently promoted malignant phenotypes of renal cancer cells, thus UCA1 playing an oncogenic role and miR-182-5p as an antioncogenic one in renal cancer pathogenesis. Conclusion: UCA1-miR-182-5p-DLL4 axis is involved in proliferation and progression of renal cancer. Thus, this study demonstrated that UCA1 plays a critical regulatory role in renal cancer cell and UCA1 may serve as a potential diagnostic biomarker and therapeutic target of renal cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

“…However, miR-182-5p is up-regulated in Oral squamous cell carcinoma, breast cancer and hepatocellular carcinoma etc. [31][32][33][34][35][36]. However, the underlying mechanisms of miR-182-5p in the malignant behaviors of RCC are unclarified.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

Wang

et al. 2020

Mol Cancer

101

View full text Add to dashboard Cite

show abstract

“…And it has been demonstrated that miR‐182 participated in tumorigenesis and metastasis; it suppresses transcription of proinflammatory genes driven by TNF‐α (Miller et al, 2016; Wei, Lei, & Hu, 2015). In addition, it also negatively regulates immune responses in Atherosclerosis via targeting TLR4 and impacts the clonal expansion of activated helper T lymphocytes (Qin, Peng, Shi, & Ke, 2018; Stittrich et al, 2010). More important, miR‐182 may have an effect on immune response, cell proliferation, inflammation, and apoptosis‐related to the therapeutic effects of BM‐MSCs in ALI (Park, Jeong, Park, Yang, & Shin, 2018).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐182 supplies negative feedback regulation to ameliorate lipopolysaccharide‐induced ALI in mice by targeting TLR4

Yang

Chen

Jiang

et al. 2020

Journal Cellular Physiology

View full text Add to dashboard Cite

Acute lung injury (ALI), characterized by increased excessive pulmonary inflammation, is a pervasive inflammatory disease with clinically high incidence. MicroRNA (miRNAs) have been associated with the progression of multiple diseases and are regarded as novel regulators of inflammation. However, it remains largely unknown whether the miRNAsmediated regulatory mechanism has an effect on lipopolysaccharide (LPS)-induced inflammation in ALI. We discovered that miR-182 distinctly lessened expression in the lung tissue of mice with ALI and macrophages stimulated by LPS. We also found that overexpression of miR-182 significantly cut down the secretion of inflammatory cytokines, while this change was reversed by inhibition of miR-182. In addition, miR-182 suppressed the activation of NF-κB by targeting TLR4 expression. And it was confirmed that miR-182 directly regulated TLR4 expression at the posttranscriptional level by binding to the 3′-UTR of TLR4. Together, these data suggested that inhibition of TLR4 expression assuaged LPS-stimulated inflammation through negative feedback regulation of miR-182. K E Y W O R D Sacute lung injury, miR-182, NF-κB, TLR4

show abstract

“…Emerging evidence suggests that miR-182-5p contribute to anti-apoptotic and antioxidative processes. MiR-182-5p inhibited oxidative stress-induced apoptosis via targeting TLR4 [18].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-182-5p protects human lens epithelial cells against oxidative stress-induced apoptosis by inhibit ing NOX4 and p38 MAPK signaling

Yuan

2020

Preprint

View full text Add to dashboard Cite

Background: MicroRNAs (miRNAs) are abnormally expressed in varying ocular diseases, including agerelated cataract. However, the roles of miR-182-5p in age-related cataract progression remains unclear.Methods: The expression of miR-182-5p in HLE-B3 cells were detected by qRT-PCR. HLE-B3 cells were transfected with miR-182-5p mimics. CCK-8, EdU, flow cytometry, 2',7'-dichlorodihydrofluorescein diacetate, JC-1 kit, and Western bolt were used to assess the cell viability, proliferation, apoptosis, reactive oxygen species (ROS) level, mitochondrial membrane potential (MMP), and protein expression, respectively, in vitro . The target relationship of miR-182-5p and NOX4 was confirmed using dual-luciferase reporter gene analysis.Results: We found that miR-182-5p was significantly decreased by the H 2 O 2 exposure.Overexpression of miR-182-5p promoted cell proliferation, inhibited ROS production and apoptosis in H 2 O 2 -induced HLE-B3 cells. Moreover, p-p-38, p-ERK, and p-JNK were up-regulated in H 2 O 2treated HLE-B3 cells, and overexpression of miR-182-5p reversed the effect of H 2 O 2 on HLE-B3cells. In addition, dual-luciferase reporter assay substantiated that NOX4 was a direct target and downregulated by miR-182-5p.Conclusions: We concluded that miR-182-5p inhibited lens epithelial cells apoptosis through regulating NOX4 and p38 MAPK signaling, providing a novel biomarker for treatment of age-related cataract.

show abstract

MiR‐182‐5p inhibited oxidative stress and apoptosis triggered by oxidized low‐density lipoprotein via targeting toll‐like receptor 4

Cited by 64 publications

References 40 publications

Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

Long non-coding RNA UCA1 promotes malignant phenotypes of renal cancer cells by modulating the miR-182-5p/DLL4 axis as a ceRNA

MicroRNA‐182 supplies negative feedback regulation to ameliorate lipopolysaccharide‐induced ALI in mice by targeting TLR4

MicroRNA-182-5p protects human lens epithelial cells against oxidative stress-induced apoptosis by inhibit ing NOX4 and p38 MAPK signaling

Contact Info

Product

Resources

About