Retraction Note to: Circular RNA circ_0003204 inhibits proliferation, migration and tube formation of endothelial cell in atherosclerosis via miR-370-3p/TGFβR2/phosph-SMAD3 axis

Zhang, Shanchao; Song, Guang-Jing; Yuan, Jing; Qiao, Shan; Xu, Shan; Si, Zhihua; Yang, Yang; Xu, Xuxu; Wang, Aihua

doi:10.1186/s12929-021-00761-3

Cited by 7 publications

(8 citation statements)

References 43 publications

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“…Accumulating evidence has suggested that circRNAs play important regulatory roles in multiple human diseases by acting as miRNA sponges 23,24 . For instance, circ_0003204 restrains endothelial cell growth, migration, and angiogenesis in atherosclerosis by sponging miR‐370‐3p 25 . Serving as a miR‐31‐5p sponge, circ‐BPTF might aggravate bladder cancer development 26 .…”

Section: Discussionmentioning

confidence: 99%

Circ_0138960 contributes to lipopolysaccharide‐induced periodontal ligament cell dysfunction

et al. 2022

Immunity Inflam & Disease

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Background: Periodontitis is a common oral inflammatory disease, and lipopolysaccharide (LPS) is a key risk factor in periodontitis pathology. Here, we used LPS-induced periodontal ligament cells (PDLCs) to explore the molecular mechanism of periodontitis. Methods: Cell viability, proliferation, and apoptosis were analyzed by Cell Counting Kit-8, 5-ethynyl-20-deoxyuridine (EDU), and flow cytometry assays, respectively. Apart from that, their targeting relationship was validated using dual-luciferase reporter and RNA-pull down. Results: Circular RNA_0138960 (circ_0138960) was notably upregulated in periodontitis sufferers (p < .001) and LPS-disposed PDLCs (p < .05). LPS exposure dampened PDLC proliferation, and promoted apoptosis and inflammation (p < .05). Circ_0138960 acted as a microRNA sponge for miR-518a-5p to affect histone deacetylase 6 (HDAC6) expression. Circ_0138960 absence-mediated protective effects in LPS-induced PDLCs were largely abrogated via silencing miR-518a-5p or HDAC6 overexpression (p < .05).Conclusion: Circ_0138960 promoted LPS-induced dysfunction in PDLCs by targeting miR-518a-5p/HDAC6 axis, which provided novel potential therapeutic targets for periodontitis.

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Section: Discussionmentioning

confidence: 99%

Circ_0138960 contributes to lipopolysaccharide‐induced periodontal ligament cell dysfunction

et al. 2022

Immunity Inflam & Disease

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“…A further study indicated that circ_0003204 is capable of inhibiting proliferation, migration, and tube formation of endothelial cells under ox‐LDL treatment. Mechanically, circ_0003204 could sponge miR‐370, and lead to the overexpression of the downstream gene TGFβR2 phosph‐SMAD3 through targeting the 3ʹ untranslated region (UTR; Zhang, Song, et al, 2020). Hsa_circ_0001445 was found lowly expressed in human coronary smooth muscle cells exposed to atherogenic conditions.…”

Section: Introductionmentioning

confidence: 99%

Silencing of circARHGAP12 inhibits the progression of atherosclerosis via miR‐630/EZH2/TIMP2 signal axis

Miao

et al. 2021

Journal Cellular Physiology

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Atherosclerosis (AS) is a common disease that seriously threatens human health.So far, the pathogenesis of AS has not been fully understood. This project investigates the effects of circARHGAP12 on AS and its regulatory mechanism. ApoE −/− knockout mice (ApoE) were adopted and reared with a high-fat diet to construct an AS model. Lentivirus was established to knock down the expression of circARHGAP12 in mice. After 12 weeks, the aorta was removed and the expression of circARHGAP12 was detected. Vascular oil red O staining was used to detect the degree of AS. The expression of inflammatory factors was detected by ELISA. Aortic smooth muscle cells (MASMCs) were cultured to evaluate the effects of cir-cARHGAP12 on the phenotype of MASMCs. RNA pull-down and luciferase assay were used to verify the downstream target genes of circARHGAP12. In addition, the effects of circARHGAP12 on MASMCs proliferation and migration were detected by MTT and transwell assay. Compared with the normal group, the expression of circARHGAP12 in the MASMCs under ox-LDL treatment was elevated, and circARHGAP12 silencing could inhibit AS in vitro and in vivo. The results of the mechanism study showed that circARHGAP12 can directly bind with miR-630. In addition, miR-630 can also target EZH2 to modulate the transcription of TIMP2 and to influence the migration of MASMCs. circARHGAP12 is upregulated in AS. Cir-cARHGAP12 knockdown can inhibit the progression of AS. This study expands on the role of circRNA in AS and provides potential targets for the treatment of AS.

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“…Circ_0005728 facilitated cell growth by modulating miR-512-3p in TNBC in vitro. 32 Additionally, some circRNAs participated in tumor development by regulating tube formation, such as circ_0003204 33 and circ-protein arginine methyltransferase 5. 34 In this research, we are the first to report that circ_0041732 promoted TNBC-associated properties.…”

Section: Discussionmentioning

confidence: 99%

Circ_0041732 regulates tumor properties of triple-negative breast cancer cells by the miR-149-5p/FGF5 pathway

Li¹,

Yin²,

Yan³

2022

Int J Biol Markers

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Background Triple-negative breast cancer (TNBC) is a subtype of breast cancers with a high recurrence and mortality. The important factors promoting the TNBC process have not been fully identified. In this research, the role of a TNBC-related circular RNA (circRNA), circ_0041732, was revealed in TNBC cell tumor properties. Methods The expression levels of circ_0041732, microRNA-149-5p (miR-149-5p) and fibroblast growth factor 5 ( FGF5) were detected by quantitative real-time polymerase chain reaction. The protein expression was determined by Western blot analysis or immunohistochemistry assay. Cell proliferation was detected by cell counting kit-8 and cell colony formation assays. Cell apoptosis was analyzed by flow cytometry and caspase-3 activity assays. Cell migration and invasion were evaluated by wound-healing and transwell invasion assays. Cell angiogenic capacity was investigated by a tube formation assay. The targeting relationship between miR-149-5p and circ_0041732 or FGF5 was identified by dual-luciferase reporter and RNA immunoprecipitation assays. The impacts of circ_0041732 knockdown on tumor formation were determined by an in vivo assay. Results Circ_0041732 and FGF5 expression were significantly upregulated, whereas miR-149-5p was downregulated in TNBC tissues and cells compared with normal breast tissues and cells, respectively. Circ_0041732 silencing inhibited TNBC cell proliferation, migration, invasion, and tube formation, but induced apoptosis. Additionally, circ_0041732 regulated TNBC cell tumor properties by binding to miR-149-5p. MiR-149-5p also modulated TNBC cell tumor properties by targeting FGF5. Furthermore, circ_0041732 knockdown hindered tumor formation in vivo. Conclusion Circ_0041732 silencing suppressed TNBC cell tumor properties by decreasing FGF5 expression through miR-149-5p. This finding demonstrated that circ_0041732 had the potential as a therapeutic target for TNBC.

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Retraction Note to: Circular RNA circ_0003204 inhibits proliferation, migration and tube formation of endothelial cell in atherosclerosis via miR-370-3p/TGFβR2/phosph-SMAD3 axis

Cited by 7 publications

References 43 publications

Circ_0138960 contributes to lipopolysaccharide‐induced periodontal ligament cell dysfunction

Circ_0138960 contributes to lipopolysaccharide‐induced periodontal ligament cell dysfunction

Silencing of circARHGAP12 inhibits the progression of atherosclerosis via miR‐630/EZH2/TIMP2 signal axis

Circ_0041732 regulates tumor properties of triple-negative breast cancer cells by the miR-149-5p/FGF5 pathway

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