Long non-coding RNA ADNCR suppresses adipogenic differentiation by targeting miR-204

Li, Mingxun; Sun, Xiaomei; Cai, Hanfang; Sun, Yujia; Plath, Martin; Li, Congjun; Lan, Xianyong; Lei, Chuzhao; Lin, Fengpeng; Bai, Yueyu; Chen, Hong

doi:10.1016/j.bbagrm.2016.05.003

Cited by 136 publications

(139 citation statements)

References 48 publications

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“…Consistent with lncRNA8975-1 being a noncoding RNA in the UCSC database, the CPC (Coding Potential Calculator) computational algorithm (http://cpc.cbi.pku.edu.cn/programs/run_cpc.jsp) [15] predicted that lncRNA8975-1 has very low coding potential (Fig. 2C) similar to MEG9, a well-documented bovine lncRNA with coding potential score of -0.80266 [16].…”

Section: Lncrna8975-1 Is Overexpressed In Hypertrophic Scar Tissue Anmentioning

confidence: 94%

The Long Non-Coding RNA LncRNA8975-1 is Upregulated in Hypertrophic Scar Fibroblasts and Controls Collagen Expression

Chen

Cao

et al. 2016

Cell Physiol Biochem

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Background/Aims: Long non-coding RNAs (lncRNAs) are thought to play crucial roles in human diseases. However, the function of lncRNAs in hypertrophic scar formation remains poorly understood. Methods: In this study, we investigated the expression of lncRNA8975-1 in hypertrophic scar tissues and fibroblasts by quantitative reverse transcription PCR (qRT-PCR). To investigate its function, overexpression and knockdown of lncRNA8975-1 were performed using lentivirus infection and Stealth RNAi transfection, respectively. Cell proliferation was detected by CCK-8 assay. The protein levels of collagens and alpha-smooth muscle actin (α-SMA) were analysed by western blot. Results: We found that lncRNA8975-1 was overexpressed in hypertrophic scar tissues and dermal fibroblasts. Overexpression of lncRNA8975-1 inhibited cell proliferation and reduced the protein expression levels of COL1A2, COL1A1, COL3A1 and α-SMA in hypertrophic scar fibroblasts, whereas knockdown of lncRNA8975-1 had the opposite effect. Conclusion: Our results show that the long non-coding RNA lncRNA8975-1 is upregulated in hypertrophic scar fibroblasts; furthermore, it inhibits fibroblast proliferation and reduces collagen and α-SMA expression. Further studies on the mechanisms regulated by lncRNA8975-1 would lead to a better understanding of the pathogenesis of hypertrophic scar formation.

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Section: Lncrna8975-1 Is Overexpressed In Hypertrophic Scar Tissue Anmentioning

confidence: 94%

The Long Non-Coding RNA LncRNA8975-1 is Upregulated in Hypertrophic Scar Fibroblasts and Controls Collagen Expression

Chen

Cao

et al. 2016

Cell Physiol Biochem

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“…Consistent with AC067945.2 being a non-coding RNA based on the UCSC database, the Coding Potential Calculator (CPC) computational algorithm (http://cpc.cbi.pku.edu.cn/programs/run_cpc.jsp) predicted that AC067945.2 has very low coding potential (Fig. 2C) similar to that of MEG9, a welldocumented bovine lncRNA with a coding potential score of -0.570863 [12,17].…”

Section: Ac0679452 Is Down-regulated In Hypertrophic Scar Tissuesmentioning

confidence: 86%

Overexpression of LncRNA AC067945.2 Down-Regulates Collagen Expression in Skin Fibroblasts and Possibly Correlates with the VEGF and Wnt Signalling Pathways

Chen¹,

Li²,

Li³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long non-coding RNAs (lncRNAs) are thought to play crucial roles in human diseases. However, the function of lncRNAs in hypertrophic scar formation remains poorly understood. Methods: Utilizing qRT-PCR, we explored the expression changes of AC067945.2. Overexpression of AC067945.2 in normal skin fibroblasts was performed by transient plasmid transfection. Western blot was used to check the proteins' expression changes. Cell Counting Kit-8 (CCK-8) assay and Annexin V/7-AAD staining were used to examine cell proliferation and apoptosis, respectively. mRNA-seq was applied to dissect the differentially expressed mRNAs in AC067945.2 overexpressed cells. We also performed ELISA to detect the VEGF secretion. Results: AC067945.2 was down-regulated in hypertrophic scar tissues. Overexpression of AC067945.2 did not affect cell proliferation, but it mildly promoted early apoptosis in normal skin fibroblasts. Furthermore, AC067945.2 overexpression inhibited the expression of COL1A1, COL1A2, COL3A1 and α-SMA proteins. Transforming growth factor-β1 (TGF-β1) could inhibit the expression of AC067945.2. Based on mRNA-seq data, compared with mRNAs in the control group, 138 mRNAs were differentially expressed, including 14 upregulated and 124 down-regulated transcripts, in the AC067945.2 overexpression group. Gene ontology and pathway analyses revealed that AC067945.2 overexpression was correlated with developmental processes, binding, extracellular region, and the vascular endothelial

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“…A recent, comprehensive survey of lncRNAs expressed differentially between bovine preadipocytes and differentiated adipocytes identified a novel lncRNA, ADNCR , that inhibits adipogenic differentiation by acting as a sponge of miR-204 [89]. Reduced expression of ADNCR with the onset of adipogenic differentiation increases free-functioning miR-204 that downregulates the target genes RUNX2 and SIRT1 [89,90].…”

Section: Functional Roles Of Lncrnas In Tgf-β- and Wnt-dependent Omentioning

confidence: 99%

“…Reduced expression of ADNCR with the onset of adipogenic differentiation increases free-functioning miR-204 that downregulates the target genes RUNX2 and SIRT1 [89,90]. Disruption of RUNX2 in knockout mice shows maturation arrest of osteoblasts [38].…”

Section: Functional Roles Of Lncrnas In Tgf-β- and Wnt-dependent Omentioning

confidence: 99%

The Roles of Long Non-Protein-Coding RNAs in Osteo-Adipogenic Lineage Commitment

Yoshioka

Yoshiko

2017

IJMS

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Osteoblasts and adipocytes share a common mesenchymal progenitor in the bone marrow. This implies that a reciprocal relationship exists between osteogenic and adipogenic differentiation. Further, cells of osteoblast lineage transdifferentiate into adipocytes under some circumstances. Dysregulation of osteo-adipogenic fate-determination leads to bone diseases such as osteoporosis, accompanied by an increase in bone marrow adipose tissue. Thus, the fine-tuning of osteo-adipogenesis is necessary for bone homeostasis. Osteo-adipogenic progression is governed by a complex crosstalk of extrinsic signals, transcription factors, and epigenetic factors. Long non-protein-coding RNAs (lncRNAs) act in part as epigenetic regulators in a broad range of biological activities, such as chromatin organization, transcriptional regulation, post-translational modifications, and histone modification. In this review, we highlight the roles of epigenetic regulators, particularly lncRNAs, in the osteo-adipogenic lineage commitment of bone marrow mesenchymal stem cells and the adipogenic transdifferentiation of osteoblasts.

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Long non-coding RNA ADNCR suppresses adipogenic differentiation by targeting miR-204

Cited by 136 publications

References 48 publications

The Long Non-Coding RNA LncRNA8975-1 is Upregulated in Hypertrophic Scar Fibroblasts and Controls Collagen Expression

The Long Non-Coding RNA LncRNA8975-1 is Upregulated in Hypertrophic Scar Fibroblasts and Controls Collagen Expression

Overexpression of LncRNA AC067945.2 Down-Regulates Collagen Expression in Skin Fibroblasts and Possibly Correlates with the VEGF and Wnt Signalling Pathways

The Roles of Long Non-Protein-Coding RNAs in Osteo-Adipogenic Lineage Commitment

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