MicroRNA-181d is a tumor suppressor in human esophageal squamous cell carcinoma inversely regulating Derlin-1

Li, Dejun; Shi, Mo; Ji, Hongsheng; Chen, Gang; Jiang, Hua; Wang, Zhou

doi:10.3892/or.2016.5028

Cited by 17 publications

(9 citation statements)

References 18 publications

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“…Micro-RNA-181d functions as an important mediator in apoptosis, proliferation, and migration of AECs by targeting Bcl2 and Derlin1 (53,85). Increased expression of miRNA-181d in AECs exposed to CSE promotes cell apoptosis mainly through inhibiting the epithelial production of Bcl2, which is an antiapoptotic protein (44,71).…”

Section: Microrna-128b and Microrna-181dmentioning

confidence: 99%

The role of noncoding RNAs in regulating epithelial responses in COPD

Chen

Thomas

Kumar

et al. 2018

American Journal of Physiology-Lung Cellular and Molecular Phys

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Chronic obstructive pulmonary disease (COPD), one of the leading causes of death in the world, is a chronic inflammatory disease of the airways usually caused by long-term exposure to inhaled irritants. Airway epithelial cells (AECs) play a key role in initializing COPD and driving the exacerbation of this disease through the release of various cytokines. This AEC-derived cytokine response is tightly regulated possibly through the regulatory effects of noncoding RNAs (ncRNAs). Although the importance of ncRNAs in pulmonary diseases has been increasingly realized, little is known about the role of ncRNA in the regulation of inflammatory responses in COPD. This review outlines the features of AEC-derived cytokine responses in COPD and how ncRNAs regulate these inflammatory responses.

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Section: Microrna-128b and Microrna-181dmentioning

confidence: 99%

The role of noncoding RNAs in regulating epithelial responses in COPD

Chen

Thomas

Kumar

et al. 2018

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Furthermore, miR-181d was found to mediate tumorigenesis and tumor development as a tumor suppressor. Ectopic expression of miR-181d suppressed cell proliferation and promoted apoptosis in osteosarcoma, colorectal cancer, gastric cancer, human esophageal squamous cell carcinoma and glioma (Wang et al, 2012;Li et al, 2016;Guo et al, 2017;Chen et al, 2018;Huang et al, 2018;Jiang et al, 2019). The expression levels of 76 miRNAs in the kidneys of mice with IRI were changed by at least two-fold, and the expression level of miR-181d was significantly decreased (Chen et al, 2004;Liu et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

MiR-181d-5p Targets KLF6 to Improve Ischemia/Reperfusion-Induced AKI Through Effects on Renal Function, Apoptosis, and Inflammation

Zhang

Chen

et al. 2020

Front. Physiol.

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Renal tubular epithelial cell (RTEC) death and renal interstitial inflammation are the most crucial pathophysiological changes in acute kidney ischemia/reperfusion injury (IRI). The microRNA (miR)-181d family plays diverse roles in cell proliferation, apoptosis and inflammation, but its renal target and potential role in IRI are unknown. Here, we showed that the expression of miR-181d-5p decreased and Krueppel-like factor 6 (KLF6) increased in a renal cell (HK-2) model of hypoxia/reoxygenation (H/R) injury and a mouse model of renal IRI. They were mainly distributed in the renal tubules. After renal IRI, miR-181d-5p overexpression significantly inhibited inflammatory mediators, reduced apoptosis and further improved renal function. KLF6 exacerbated RTEC damage and acted as a NF-κB co-activator to aggravate the renal IRI inflammatory response. Mechanistically, KLF6 was predicted as a new potential target gene of miR-181d-5p through bioinformatic analysis and luciferase reporter assay verification. After overexpressing miR-181d-5p and inhibiting KLF6, the role of miR-181d-5p was weakened on the renal damage improvement. In conclusion, miR-181d-5p upregulation produced protective antiapoptotic and anti-inflammatory effects against IRI in kidneys in vivo and H/R injury in HK-2 cells in vitro, and these effects were achieved by targeted inhibition of KLF6. Thus, our results provide novel insights into the molecular mechanisms associated with IRI and a potential novel therapeutic target.

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“…DERL1 is a partner of the p97 ATPase complex and plays a key role in the mislocalization of the misfolded protein; it also integrates into the endoplasmic reticulum (ER) membrane to survey such protein aggregates [16, 17]. Recently, several studies have demonstrated that DERL1 contributes to carcinogenesis and tumor progression, and the upregulation of DERL1 expression promotes the development of colon cancer, esophageal cancer, and bladder cancer [18-20]. In addition, DERL1 is consistently overexpressed in NSCLC and correlated with tumor grade and lymph node metastasis.…”

Section: Introductionmentioning

confidence: 99%

MiR-598 Suppresses Invasion and Migration by Negative Regulation of Derlin-1 and Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer

Yang

Wei

Qin

et al. 2018

Cell Physiol Biochem

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Background/Aims: MicroRNAs regulate a wide range of biological processes of non-small cell lung cancer (NSCLC). Although miR-598 has been reported to act as a suppressor in osteosarcoma and colorectal cancer, the physiological function of miR-598 in NSCLC remains unknown. In this study, the role of miR-598 in NSCLC was investigated. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to estimate the expression of miR-598 and Derlin-1 (DERL1) in both NSCLC tissues and cell lines. Immunohistochemistry (IHC) analyzed the association between the miR-598 expression and epithelial-mesenchymal transition (EMT) hallmark genes (E-cadherin, Vimentin) by staining the tumors representative of the high- and low-expression groups. The effect of miR-598 and DERL1 on invasion and migration was determined in vitro using transwell and wound-healing assays. The molecular mechanism underlying the relevance between miR-598 and DERL1 was elucidated by luciferase assay and Western blot. Western blot assessed the expression levels of EMT hallmark genes in cell lines. Xenograft tumor formation assay was conducted as an in vivo experiment. Results: In this study, a relatively low level of miR-598 and high DERL1 expressions were found in NSCLC specimens and cell lines. IHC results established a positive correlation between the miR-598 expression and E-cadherin and a negative with Vimentin. DERL1 was verified as a direct target of miR-598 by luciferase assay. In vitro, the over-expression of miR-598 negatively regulated DERL1 and EMT for the suppression of invasion and migration. In vivo, the over-expression of miR-598 could inhibit tumor cell metastasis in NSCLC. Conclusions: These findings for the first time revealed that miR-598, as a tumor suppressor, negatively regulate DERL1 and EMT to suppress the invasion and migration in NSCLC, thereby putatively serving as a novel therapeutic target for NSCLC clinical treatment.

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MicroRNA-181d is a tumor suppressor in human esophageal squamous cell carcinoma inversely regulating Derlin-1

Cited by 17 publications

References 18 publications

The role of noncoding RNAs in regulating epithelial responses in COPD

The role of noncoding RNAs in regulating epithelial responses in COPD

MiR-181d-5p Targets KLF6 to Improve Ischemia/Reperfusion-Induced AKI Through Effects on Renal Function, Apoptosis, and Inflammation

MiR-598 Suppresses Invasion and Migration by Negative Regulation of Derlin-1 and Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer

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