RETRACTED: LNCRNA CDKN2B-AS1 regulates mesangial cell proliferation and extracellular matrix accumulation via miR-424-5p/HMGA2 axis

Li, Yang; Zheng, Linlin; Huang, Denggao; Cao, Hui; Gao, Yuanhui; Fan, Zhongcheng

doi:10.1016/j.biopha.2019.109622

Cited by 33 publications

(25 citation statements)

References 37 publications

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“…A number of publications have reported that lncRNAs are directly related to the pathophysiological development of DN [28,29]. For example, knockdown of CDKN2B-AS1 suppressed mesangial cell proliferation and ECM accumulation through the miR-424-5p/ HMGA2 axis [30]. A previous study discovered the correlation between CASC2 and the diagnosis and prognosis of patients suffering from DN [15].…”

Section: Discussionmentioning

confidence: 99%

LncRNA CASC2 Alleviates the Progression of Diabetic Nephropathy by Regulating the miR-144/SOCS2 Signalling Axis

Min

Xie

2020

Kidney Blood Press Res

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Background: Diabetic nephropathy constitutes a large proportion of end-stage kidney failure in diabetic patients. However, the underlying molecular mechanisms remain unclear. Methods: Db/db diabetic mouse models and high glucose (HG)-induced human renal mesangial cells (HRMCs) were used as research models in vivo and in vitro. The expression of cancer susceptibility candidate 2 (CASC2) was quantified by qRT-PCR. The regulatory role of CASC2 in cell apoptosis, inflammatory factor release, and fibrosis was verified by flow cytometry, qRT-PCR, and Western blot assay, respectively. The bioinformatics prediction software DIANA and starBase v2.0 were used to predict the putative binding sites. The interactions among CASC2, miR-144, and SOCS2 were explored by the luciferase assay and Western bolt assay. Results: The expression of CASC2 in diabetic mouse models and HG-induced HRMCs was lower than that in the control (p < 0.05). Overexpression of CASC2 resulted in a decrease in the apoptosis rate, inflammatory factor release (TNF-α, IL-6, and IL-1β), expression of cleaved caspase-3, and fibrotic proteins (fibronectin, Col-IV, and TGF-β1) and an increase in Bcl-2 expression. Inhibition of CASC2 caused increased expression of miR-144. Furthermore, mechanistic investigations confirmed that activation of the miR-144/SOCS2 regulatory loop by overexpression of miR‐144 reversed the in vitro effects of CASC2 on inhibiting cell apoptosis, inflammatory factor release, and fibrosis. In addition, simultaneous overexpression of miR-144 and SOCS2 further increased the inhibition of cell apoptosis, inflammatory factor release, and fibrosis by CASC2. Conclusion: CASC2 could alleviate the degree and process of apoptosis, inflammation, and fibrosis in diabetic nephropathic models by regulating the miR-144/SOCS2 axis.

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Section: Discussionmentioning

confidence: 99%

LncRNA CASC2 Alleviates the Progression of Diabetic Nephropathy by Regulating the miR-144/SOCS2 Signalling Axis

Min

Xie

2020

Kidney Blood Press Res

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“…Herein, CDKN2B-AS1 silencing decreased viability, ECM accumulation, inflammation response, and induced cell cycle arrest of HG-induced HMCs. Li et al revealed that CDKN2B-AS1 silencing curbed ECM accumulation and proliferation of HG-induced HMCs through regulating the miR-424-5p/HMGA2 pathway in DN [17]. Also, CDKN2B-AS1 interference played a protective effect on diabetic mouse kidneys [16].…”

Section: Discussionmentioning

confidence: 99%

“…Accumulated researches have proved that CDKN2B-AS1 takes part in the regulation of the gene expression via serving as a ceRNA [17,30]. One report claimed that miR-15b-5p could reduce HG-induced podocyte injury by repressing inflammation response, oxidative stress, and apoptosis of podocyte via downregulating Sema3A [22].…”

Section: Discussionmentioning

confidence: 99%

“…Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) has been reported to be implicated in tumor advancement [13], atherosclerosis [14], cerebral infarction [15], diabetes [16], and so on. It has been revealed that CDKN2B-AS1 contributes to the progression of DN [16,17]. However, the regulatory mechanisms of CDKN2B-AS1 in DN have not been completely clarified.…”

Section: Introductionmentioning

confidence: 99%

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Long non-coding RNA CDKN2B-AS1 regulates high glucose-induced human mesangial cell injury via regulating the miR-15b-5p/WNT2B axis

Chang

Fang

et al. 2020

Diabetol Metab Syndr

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Background Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) has been reported to be related to diabetic nephropathy (DN) progression. However, the regulatory mechanisms of CDKN2B-AS1 in DN are unclear. Methods High glucose (HG) was used to induce human mesangial cells (HMCs) for establishing the DN model. Expression levels of CDKN2B-AS1, microRNA (miR)-15b-5p, wingless-Type family member 2B (WNT2B) mRNA in serum and HMCs were detected through quantitative real-time polymerase chain reaction (qRT-PCR). The viability and cell cycle progression of HMCs were determined with Cell Counting Kit-8 (CCK-8) or flow cytometry assays. The levels of several proteins and inflammatory factors in HMCs were analyzed by western blotting or enzyme-linked immunosorbent assay (ELISA). The relationship between CDKN2B-AS1 or WNT2B and miR-15b-5p was verified with dual-luciferase reporter assay. Results CDKN2B-AS1 and WNT2B were upregulated while miR-15b-5p was downregulated in serum of DN patients and HG-treated HMCs. CDKN2B-AS1 inhibition reduced HG-induced viability, cell cycle progression, ECM accumulation, and inflammation response in HMCs. CDKN2B-AS1 regulated WNT2B expression via competitively binding to miR-15b-5p. MiR-15b-5p inhibitor reversed CDKN2B-AS1 knockdown-mediated influence on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs. The repressive effect of miR-15b-5p mimic on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs was abolished by WNT2B overexpression. Conclusion CDKN2B-AS1 regulated HG-induced HMC viability, cell cycle progression, ECM accumulation, and inflammation response via regulating the miR-15b-5p/WNT2B axis, provided a new mechanism for understanding the development of DN.

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“…In previous studies, a number of antisense RNAs has been revealed to affect the cell phenotypes by modulating the PI3K/AKT pathway. 38,39 Thus, we investigated the hypothesis that TBX5-AS1 might regulate the PI3K/AKT pathway in NSCLC cells. As results, we found that TBX5-AS1 overexpression suppressed the phosphorylation of PI3K and AKT, indicating that TBX5-AS1 might inactivate the PI3K/AKT pathway.…”

Section: Dovepressmentioning

confidence: 99%

LncRNA TBX5-AS1 Regulates the Tumor Progression Through the PI3K/AKT Pathway in Non-Small Cell Lung Cancer

Qing-hai¹,

Jiang²,

Li³

2020

OTT

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Long non-coding RNAs (lncRNAs) have been reported to play important roles in tumor biology. In this study, we aimed to investigate the effects of T-box transcription factor 5 antisense RNA 1 (TBX5-AS1) on aggressive phenotypes of non-small cell lung cancer (NSCLC) cells and explore its regulatory pathway. Methods: The expression of TBX5-AS1 in tissues, plasma, and cells was determined by qRT-PCR. Cell viability, proliferation, migration, invasion, and apoptosis were assessed using MTT, colony formation, wound-healing, Transwell, and flow cytometry assay, respectively. Western blot analysis was performed to measure the expression of apoptosis-related proteins. Besides, transfected cells were exposed to PI3K activator (740Y-P) to verify the regulatory pathway. Results: TBX5-AS1 expression was down-regulated in NSCLC tissues, plasma, and cells, and associated with lymph node metastasis and histological grade. Overexpression of TBX5-AS1 inhibited cell viability, colony formation, migration, and invasion, while it promoted apoptosis. Conversely, knockdown of TBX5-AS1 showed the completely opposite results. Additionally, western blot showed that the phosphorylation of PI3K and AKT was stimulated by TBX5-AS1 knockdown and suppressed by TBX5-AS1 overexpression. The addition of 740Y-P in transfected cells reversed the TBX5-AS1induced inhibition of PI3K and AKT phosphorylation and effects on aggressive phenotypes of NSCLC cells. Conclusion: The study confirmed the down-regulation of TBX5-AS1 in patients with NSCLC and its association with the progression. We innovatively proposed a possible model of TBX5-AS1-mediated gene regulation in NSCLC progression that TBX5-AS1 inhibited the aggressive phenotypes of NSCLC cells through inactivating the PI3K/AKT pathway. This finding provided a novel insight into NSCLC pathogenesis.

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RETRACTED: LNCRNA CDKN2B-AS1 regulates mesangial cell proliferation and extracellular matrix accumulation via miR-424-5p/HMGA2 axis

Cited by 33 publications

References 37 publications

LncRNA CASC2 Alleviates the Progression of Diabetic Nephropathy by Regulating the miR-144/SOCS2 Signalling Axis

LncRNA CASC2 Alleviates the Progression of Diabetic Nephropathy by Regulating the miR-144/SOCS2 Signalling Axis

Long non-coding RNA CDKN2B-AS1 regulates high glucose-induced human mesangial cell injury via regulating the miR-15b-5p/WNT2B axis

<p>LncRNA <em>TBX5-AS1</em> Regulates the Tumor Progression Through the PI3K/AKT Pathway in Non-Small Cell Lung Cancer</p>

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