RETRACTED ARTICLE: Involvement of NORAD/miR-608/STAT3 axis in carcinostasis effects of physcion 8-O-β-glucopyranoside on ovarian cancer cells

Yang, Xiaohong; Yan, Yimin; Chen, Yuhuan; Li, Jingwen; Yang, Jing

doi:10.1080/21691401.2019.1637884

Cited by 22 publications

(15 citation statements)

References 43 publications

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“…However, the role of NORAD in DR has not been reported. Previously, Yang et al proved that NORAD/miR-608/STAT3 axis in carcinostasis effects the physcion 8-O-bglucopyranoside on ovarian cancer cells [23], implying the near correlation between miR-608 and NORAD. Currently, few reports were focussed on miR-608 in DR. To the contrary, miR-125 was found in DR in the HG-disposed condition, and it can be associated with cell apoptosis under HG-disposed condition [24].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ATICLE: Physcion 8-O-β-glucopyranoside exerts protective roles in high glucose-induced diabetic retinopathy via regulating lncRNA NORAD/miR-125/STAT3 signalling

Wan

Long

et al. 2020

Artificial Cells, Nanomedicine, and Biotechnology

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2020) Physcion 8-O-β-glucopyranoside exerts protective roles in high glucose-induced diabetic retinopathy via regulating lncRNA NORAD/miR-125/ STAT3 signalling, Artificial ABSTRACT Diabetic retinopathy (DR) is the leading cause of decreased vision and blindness globally. The aim of this study was to understand the role of physcion 8-O-b-glucopyranoside (PG) in high glucose (HG)induced DR and to investigate whether lncRNA NORAD/miR-125/STAT3 signalling was the underlying mechanism involved in DR. To this end, the serum levels of NORAD, miR-125, and STAT3 were determined in patients with DR. The APRE-19 cells were subjected to HG treatment to construct the cell model of DR. HG-disposed APRE-19 cell injury was assessed by detecting cell viability, apoptosis, concentrations of pro-inflammatory cytokines including TNF-a and IL-1b, and ROS generation. Moreover, the effect of PG on HG-disposed APRE-19 cell injury was investigated. NORAD was then overexpressed to investigate the combined effects of NORAD overexpression and PG on HG-disposed APRE-19 cell injury. Furthermore, the regulatory relationship between NORAD and miR-125 as well as miR-125 and STAT3 was investigated. The expression levels of NORAD and STAT3 were significantly increased in the serum of DR patients, while the miR-125 expression was decreased. The HG treatment-induced injury to APRE-19 cells, which were alleviated by PG treatment. Moreover, PG alleviated HG-disposed injury to ARPE-19 cells by decreasing NORAD. NORAD negatively regulated miR-125 expression and the combined effects of NORAD and PG on HG-disposed ARPE-19 cell injury were reversed by miR-125 overexpression. Furthermore, STAT3 was confirmed as a target gene of miR-125. Our results show that PG exerts protective roles in HG-disposed DR via regulating lncRNA NORAD/miR-125/STAT3 signalling. NORAD/miR-125/STAT3 axis may provide a novel perspective for target therapy of DR. ARTICLE HISTORY

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Section: Introductionmentioning

confidence: 99%

RETRACTED ATICLE: Physcion 8-O-β-glucopyranoside exerts protective roles in high glucose-induced diabetic retinopathy via regulating lncRNA NORAD/miR-125/STAT3 signalling

Wan

Long

et al. 2020

Artificial Cells, Nanomedicine, and Biotechnology

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“…To date, the roles of NORAD in diseases have been mainly focused on its effects on tumors. For example, NORAD could promote the development of ovarian cancer, gastric cancer, and pancreatic cancer colorectal cancer [21][22][23][24]. No studies have been reported on the effects of NORAD on endothelial cell injury and atherosclerosis.…”

Section: Agingmentioning

confidence: 99%

Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis

Bian

Jing

Yang

et al. 2020

Aging

120

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Long noncoding RNAs (lncRNAs) play important roles in the development of vascular diseases. However, the effect of lncRNA NORAD on atherosclerosis remains unknown. This study aimed to investigate the effect NORAD on endothelial cell injury and atherosclerosis. Ox-LDL-treated human umbilical vein endothelial cells (HUVECs) and high-fat-diet (HFD)-fed ApoE −/− mice were used as in vitro and in vivo models. Results showed that NORAD-knockdown induced cell cycle arrest in G0/G1 phase, aggravated ox-LDL-induced cell viability reduction, cell apoptosis, and cell senescence along with the increased expression of Bax, P53, P21 and cleaved caspase-3 and the decreased expression of Bcl-2. The effect of NORAD on cell viability was further verified via NORAD-overexpression. NORAD-knockdown increased ox-LDL-induced reactive oxygen species, malondialdehyde, p-IKBα expression levels and NF-κB nuclear translocation. Proinflammatory molecules ICAM, VCAM, and IL-8 were also increased by NORAD-knockdown. Additionally, we identified the strong interaction of NORAD and IL-8 transcription repressor SFPQ in HUVECs. In ApoE −/− mice, NORAD-knockdown increased the lipid disorder and atherosclerotic lesions. The results have suggested that lncRNA NORAD attenuates endothelial cell senescence, endothelial cell apoptosis, and atherosclerosis via NF-κB and p53-p21 signaling pathways and IL-8, in which NORAD-mediated effect on IL-8 might through the direct interaction with SFPQ.

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“…Several studies have revealed that NORAD had effects on tumor cell proliferation, apoptosis, and migration via binding with miRNAs or proteins 13 . NORAD was identified as an oncogene in pancreatic and ovarian cancer 14,15 , while its roles in lung and breast cancers have been controversial, indicating a context-dependent role in cancer progression 16 . The function and mechanism of NORAD involved in regulating EC formation and progression remain unexplored.…”

Section: Introductionmentioning

confidence: 99%

NORAD orchestrates endometrial cancer progression by sequestering FUBP1 nuclear localization to promote cell apoptosis

Han

et al. 2020

Cell Death Dis

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Long noncoding RNAs (lncRNAs) are emerging as critical regulators in tumor initiation and progression. However, the biological mechanisms and potential clinical application of lncRNA NORAD in endometrial cancer (EC) remain unknown. Herein, we identified NORAD underwent promoter hypermethylation-associated downregulation in EC. Epigenetic inactivation of NORAD was correlated with EC progression (FIGO stage) and poor outcome. Overexpression of NORAD significantly inhibited cell growth and promoted apoptosis in EC cells. Mechanistic studies revealed that multiple regions of NORAD served as a platform for binding with the central domain of anti-apoptotic factor FUBP1. Our findings further indicated that the NORAD/FUBP1 interaction attenuated FUBP1 nuclear localization and thus impaired the occupancies of FUBP1 on its target pro-apoptotic gene promoters, resulting in apoptosis induction in EC. Moreover, knockdown of NORAD promoted tumor growth in the xenograft mice model. While, introduction of NORAD-4 fragment, which bound with FUBP1, successfully reversed tumor growth and apoptosis inhibition mediated by NORAD knockdown in vivo. Our findings provide mechanistic insight into the critical roles of NORAD as a tumor suppressor in EC progression. NORAD could possibly serve as a novel prognostic biomarker and provide the rationale for EC therapy.

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RETRACTED ARTICLE: Involvement of NORAD/miR-608/STAT3 axis in carcinostasis effects of physcion 8-O-β-glucopyranoside on ovarian cancer cells

Cited by 22 publications

References 43 publications

RETRACTED ATICLE: Physcion 8-O-β-glucopyranoside exerts protective roles in high glucose-induced diabetic retinopathy via regulating lncRNA NORAD/miR-125/STAT3 signalling

RETRACTED ATICLE: Physcion 8-O-β-glucopyranoside exerts protective roles in high glucose-induced diabetic retinopathy via regulating lncRNA NORAD/miR-125/STAT3 signalling

Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis

NORAD orchestrates endometrial cancer progression by sequestering FUBP1 nuclear localization to promote cell apoptosis

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