Circ_0068655 Promotes Cardiomyocyte Apoptosis via miR-498/PAWR Axis

Chai, Qiaoying; Zheng, Mingqi; Wang, Le; Mei, Wei; Yin, Yajuan; Ma, Fangfang; Li, Xinping; Zhang, Haijun; Li, Gang

doi:10.1007/s13770-020-00270-8

Cited by 23 publications

(24 citation statements)

References 29 publications

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“…This may also be due to apoptosis induction by MIR9-3HG silencing. Certain studies have showed that miR-498 affects cell apoptosis, potentially via regulating mitochondria-mediated apoptosis-associated proteins, such as caspase-3, Bax and Bcl-2 ( 26 , 27 ). Based on the present results and previous literature, it was hypothesized that the regulation of apoptosis via MIR9-3HG/miR-498 in cervical cancer cells may be mediated by affecting the mitochondria-mediated apoptosis pathway.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of MIR9‑3HG inhibits proliferation and promotes apoptosis of cervical cancer cells by miR‑498 via EP300

Ying

2021

Mol Med Rep

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cervical cancer is a serious gynecological cancer and one of the primary causes of mortality in female patients with cancer. despite advances in cancer research, the molecular mechanism underlying cancer remains poorly understood. High levels of Mir9-3 host gene (HG) are associated with the occurrence and development of cervical cancer. However, the specific role of MIR9-3HG during the development of cervical cancer is unclear. in the present study, the expression of Mir9-3HG was silenced in c33a and SiHa cervical cancer cell lines. Proliferation and apoptosis were measured in these cells using 5-ethynyl-2'-deoxyuridine assay and flow cytometry, respectively. In addition, targeting micrornas (mirs) of Mir9-3HG and mrnas of mir-498 were predicted using public databases. The predicted interactions between these molecules were validated using rna immunoprecipitation, rna pull-down and luciferase reporter assays. lastly, c33a cells transfected with short hairpin Mir-3HG alone or in combination with mir-498 inhibitor or Pc-eP300 were subcutaneously injected into mice. The levels of mir-498, eP300 and Ki67 in tumor tissue were measured via reverse transcription-quantitative Pcr or western blotting. Mir9-3HG knockdown inhibited the proliferation of cervical cancer cells, whilst promoting apoptosis. Mir9-3HG sponged mir-498 and inhibited its expression. additionally, mir-498 interacted with eP300 and inhibited its expression. Transfection with miR-498 inhibitor significantly decreased apoptosis levels; this effect was abolished following eP300 silencing in vitro. In vivo, both mir-498 inhibition and eP300 overexpression reversed the inhibition of tumor growth mediated by Mir-3HG knockdown. Mir9-3HG promoted the proliferation cervical cancer cells via eP300 and mir-498. These in vitro and in vivo findings demonstrate the regulatory role of the Mir9-3HG/mir-498/eP300 axis in cervical cancer cell growth. Thus, the present study identified novel molecular targets for the diagnosis and treatment of cervical cancer and provided new insight into the pathogenesis of cervical cancer.

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Section: Discussionmentioning

confidence: 99%

Knockdown of MIR9‑3HG inhibits proliferation and promotes apoptosis of cervical cancer cells by miR‑498 via EP300

Ying

2021

Mol Med Rep

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“…circRNA Ttc3 mediates cardiac function after MI by targeting miR-15b ( Cai et al, 2019 ). Circ_0068655 enhances cardiomyocyte apoptosis by miR-498/PAWR signaling ( Chai et al, 2020 ). In this study, we first identified that the expression of circPostn was elevated in the plasma of MI patients and MI rat models.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA POSTN Promotes Myocardial Infarction-Induced Myocardial Injury and Cardiac Remodeling by Regulating miR-96-5p/BNIP3 Axis

Cheng

Wang

et al. 2021

Front. Cell Dev. Biol.

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Myocardial infarction (MI) is the most prevalent cardiac disease with high mortality, leading to severe heart injury. Circular RNAs (circRNAs) are a new type of regulatory RNAs and participate in multiple pathological cardiac progressions. However, the role of circRNAs Postn (circPostn) in MI modulation remains unclear. Here, we aimed to explore the effect of circPostn on MI-induced myocardial injury and cardiac remodeling. We identified that the expression of circPostn was elevated in the plasma of MI patients, MI mouse model, and hypoxia and reoxygenation (H/R)-treated human cardiomyocytes. The depletion of circPostn significantly attenuated MI-related myocardium injury and reduced the infarct size in MI mouse model. The circPostn knockdown obviously enhanced left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) and inhibited left ventricular anterior wall thickness at diastole (LVAWd) and left ventricular posterior wall thickness at diastole (LVPWd). The depletion of circPostn was able to decrease MI-induced expression of collagen 1α1 and collagen 3α1 in the ventricular tissues of mice. The protein expression of collagen and α-smooth muscle actin (SMA) was up-regulated in MI mice and was inhibited by circPostn knockdown. Meanwhile, the expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) was repressed by circPostn depletion in the ventricular tissues of MI mice. Besides, the circPostn depletion attenuated cardiomyocyte apoptosis in mice. Mechanically, circPostn served as a miR-96-5p sponge and miR-96-5p-targeted BNIP3 in human cardiomyocytes, in which circPostn up-regulated BNIP3 expression by targeting miR-96-5p. circPostn promoted H/R-induced cardiomyocyte injury by modulating miR-96-5p/BNIP3 axis. Thus, we conclude that circPostn contributes to MI-induced myocardial injury and cardiac remodeling by regulating miR-96-5p/BNIP3 axis. Our finding provides new insight into the mechanism by which circPostn regulates MI-related cardiac dysfunction. circPostn, miR-96-5p, and BNIP3 are potential targets for the treatment of MI-caused heart injury.

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“…Moreover, circ-0068655 can contribute to hypoxia-induced apoptotic death and impairment of cell migration via the circ-0068655/miR-498/protein serine/threonine kinase (PRKC) apoptosis WT1 transcription factor (WT1) regulator (PAWR) regulatory axis. 100 Additionally, Zhai’s group 32 demonstrated that enhanced expression of circ-0060745 aggravates cell apoptosis by decreasing Bcl-2 expression and increasing Bax expression and that knockdown of circ_0060745 suppresses hypoxia-induced cardiomyocyte apoptosis through inhibition of nuclear factor κB (NF-κB) activation. Moreover, researchers found that circ-0010729 sponges miR-27a-3p, evokes tumor necrosis factor receptor (TNFR)-associated factor 5 (TRAF5) expression, and then aggravates hypoxia-induced cardiomyocyte apoptosis and injury.…”

Section: Circrnas and Cardiomyocyte Apoptosismentioning

confidence: 99%

“…For example, circRNA MFACR, circ_0062389, circ-0068655, circ_0010729, circRNA ACAP2, circ_0124644, circROBO2, circMACF1, and circArhgap12 may exert potential anti-apoptotic effects to inhibit AMI progression. 33 , 94 , 100 , 101 , 104 , 105 , 107 , 108 , 111 , 116 In addition, circRNA ACR may have an effective anti-autophagic effect. 120 During infarct healing, circHelz can exert anti-inflammatory effects, 122 circCDYL and circFASTKD1 are likely to contribute to proliferation and proangiogensis, 123 , 127 and circUbe3a can exert anti-fibrotic effects.…”

Section: Circrna-based Approaches As Potential Therapeutic Strategies For MImentioning

confidence: 99%

Emerging roles of circRNAs in the pathological process of myocardial infarction

Wen

Hui

Wang

et al. 2021

Molecular Therapy - Nucleic Acids

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Myocardial infarction (MI) is defined as cardiomyocyte death in a clinical context consistent with ischemic insult. MI remains one of the leading causes of morbidity and mortality worldwide. Although there are a number of effective clinical methods for the diagnosis and treatment of MI, further investigation of novel biomarkers and molecular therapeutic targets is required. Circular RNAs (circRNAs), novel non-coding RNAs, have been reported to function mainly by acting as microRNA (miRNA) sponges or binding to RNA-binding proteins (RBPs). The circRNA-miRNA-mRNA (protein) regulatory pathway regulates gene expression and affects the pathological mechanisms of various diseases. Undoubtedly, a more comprehensive understanding of the relationship between MI and circRNA will lay the foundation for the development of circRNA-based diagnostic and therapeutic strategies for MI. Therefore, this review summarizes the pathophysiological process of MI and various approaches to measure circRNA levels in MI patients, tissues, and cells; highlights the significance of circRNAs in the regulation MI pathogenesis and development; and provides potential clinical insight for the diagnosis, prognosis, and treatment of MI.

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Circ_0068655 Promotes Cardiomyocyte Apoptosis via miR-498/PAWR Axis

Cited by 23 publications

References 29 publications

Knockdown of MIR9‑3HG inhibits proliferation and promotes apoptosis of cervical cancer cells by miR‑498 via EP300

Knockdown of MIR9‑3HG inhibits proliferation and promotes apoptosis of cervical cancer cells by miR‑498 via EP300

Circular RNA POSTN Promotes Myocardial Infarction-Induced Myocardial Injury and Cardiac Remodeling by Regulating miR-96-5p/BNIP3 Axis

Emerging roles of circRNAs in the pathological process of myocardial infarction

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