KCNQ1OT1 promotes melanoma growth and metastasis

Guo, Bingyu; Zhang, Qian; Wang, Hongyi; Chang, Peng; Tao, Kai

doi:10.18632/aging.101418

Cited by 41 publications

(38 citation statements)

References 25 publications

(18 reference statements)

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“…Kcnq1ot1 was also proved to act as a ceRNA, targeting miRNAs to regulate the expression of mRNAs. Guo et al [27] suggested that Kcnq1ot1 could regulate MET expression to promote melanoma growth via binding to miR-153. In our study, the bioinformatics assay predicted that miR-214-3p was a ceRNA of Kcnq1ot1 and had binding sites for both Kcnq1ot1 and caspase-1, which was consistent with the results of previous study on cataracts [18].…”

Section: Discussionmentioning

confidence: 99%

LncRNA KCNQ1OT1 Mediates Pyroptosis in Diabetic Cardiomyopathy

Yang

Qin

Wang

et al. 2018

Cell Physiol Biochem

119

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Background/Aims: Diabetic cardiomyopathy (DCM) is a common complication of diabetes and can cause heart failure, arrhythmia and sudden death. The pathogenesis of DCM includes altered metabolism, mitochondrial dysfunction, oxidative stress, inflammation, cell death and extracellular matrix remodeling. Recently, pyroptosis, a type of programmed cell death related to inflammation, was proven to be activated in DCM. However, the molecular mechanisms underlying pyroptosis in DCM remain elusive. The long non-coding RNA (lncRNA) Kcnq1ot1 participates in many cardiovascular diseases. This study aims to clarify whether Kcnq1ot1 affects cardiac pyroptosis in DCM. Methods: AC16 cells and primary cardiomyocytes were incubated with 5.5 and 50 mmol/L glucose. Diabetic mice were induced with streptozotocin (STZ). Kcnq1ot1 was silenced both in vitro and in vivo. qRT-PCR was used to detect the expression level of Kcnq1ot1. Immunofluorescence, qRT-PCR and western blot analyses were used to detect the degree of pyroptosis. Echocardiography, hematoxylin and eosin staining, and Masson’s trichrome staining were used to detect the cardiac function and morphology in mice. Cell death and function were detected using TUNEL staining, immunofluorescence staining and Ca²⁺ measurements. Results: The expression of Kcnq1ot1 was increased in patients with diabetes, high glucose-induced cardiomyocytes and diabetic mouse cardiac tissue. Silencing Kcnq1ot1 alleviated pyroptosis by targeting miR-214-3p and caspase-1. Furthermore, silencing Kcnq1ot1 reduced cell death, cytoskeletal structure abnormalities and calcium overload in vitro and improved cardiac function and morphology in vivo. Conclusion: Kcnq1ot1 is overexpressed in DCM, and silencing Kcnq1ot1 inhibits pyroptosis by influencing miR-214-3p and caspase-1 expression. We clarified for the first time that Kcnq1ot1 could be a new therapeutic target for DCM.

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Section: Discussionmentioning

confidence: 99%

LncRNA KCNQ1OT1 Mediates Pyroptosis in Diabetic Cardiomyopathy

Yang

Qin

Wang

et al. 2018

Cell Physiol Biochem

119

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“…According to previous reports, through competitive binding with miRNA, mRNAs and lncRNAs could affect the native function of their binding targets (Zhou et al, ). LncRNA from KCNQ1OT1 gene has been reported as regulating imprinting of target genes at the 11p15.5 locus; and it might inhibit tumor development and/or progression in many cancers (W. Gong et al, ; B. Guo, Zhang, Wang, Chang, & Tao, ). A recent study shows that KCNQ1OT1 could promote cataract formation (Chen et al, ; Jin et al, ).…”

Section: Discussionmentioning

confidence: 99%

KCNQ1OT1 affects the progression of diabetic retinopathy by regulating miR‐1470 and epidermal growth factor receptor

Shao

Yin

Fan

et al. 2019

Journal Cellular Physiology

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Long noncoding RNAs have been reported to play important roles in the pathogenesis of diabetic retinopathy (DR), which has been considered as the most common disease leading to vision loss. However, it is still unclear whether KCNQ1 overlapping transcript 1 (KCNQ1OT1) could affect DR. In this study, regarding quantitative reverse transcription polymerase chain reaction assay, KCNQ1OT1 level was upregulated while microRNA‐1470 (miR‐1470) was decreased in DR patients and human retinal endothelial cells. High KCNQ1OT1 expression was correlated with DR stage and low visual function. Using miR‐1470 mimic or knockdown of KCNQ1OT1 could lead to the similar phenomenon; phospho‐AKT, Bax, B‐cell lymphoma 2, and cleaved poly‐ADP ribose polymerase (PARP) were regulated, while vascularization was inhibited and apoptosis was promoted. Regarding bioinformatics analysis and in vitro dual luciferase reporter assay, there should be a negative correlation between KCNQ1OT1 and miR‐1470. Additionally, mRNA of epidermal growth factor receptor (EGFR) was proved as the target of miR‐1470 and EGFR targeting by miR‐1470 initiated KCNQ1OT1 deficiency‐induced apoptosis and promoted proliferation. KCNQ1OT1 and miR‐1470 were proved to be the promoter and repressor of EGFR, respectively. The results suggested that KCNQ1OT1 could sponge miR‐1470 and further regulate EGFR in DR.

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“…KCNQ1OT1, known as potassium voltage‐gated channel subfamily Q member 1 (Kcnq1) overlapping transcript 1 or Kcnq1 opposite strand/antisense transcript 1, is an antisense LncRNA. Recently, increasing evidence suggested that KCNQ1OT1 played an important role in tumorigenesis and metastasis of different cancers . Dong et al revealed KCNQ1OT1 promoted NSCLC progression partly via sponging miR‐27b‐3p in order to target 3′‐untranslated region (3′‐UTR) of HSP90AA1 directly …”

Section: Main Molecular Mechanism Of Lncrna To Regulate the Metastasimentioning

confidence: 99%

Long non‐coding RNAs: How to regulate the metastasis of non–small‐cell lung cancer

Fang

Wang

Gong

et al. 2020

J Cellular Molecular Medi

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Non–small‐cell lung cancer (NSCLC) has become the most lethal human cancer because of the high rate of metastasis. Hence, clarifying the molecular mechanism underlying NSCLC metastasis is very important to improve the prognosis of patients with NSCLC. Long non‐coding RNAs (LncRNAs) are a class of RNA molecules longer than 200 nucleotides, which can participate in diverse biological processes. About 18% of human LncRNAs were recently found to be associated with tumours. Many studies indicated that aberrant expression of LncRNAs played key roles in the progression and metastasis of NSCLC. According to the function in tumours, LncRNAs can be divided into two classes: oncogenic LncRNAs and tumour‐suppressor LncRNAs. In this review, we summarized the main molecular mechanism of LncRNAs regulating NSCLC metastasis, including three aspects: (a) LncRNAs interact with miRNAs as ceRNAs; (b) LncRNAs bind with target proteins; and (c) LncRNAs participate in the transduction of different signal pathways. Then, LncRNAs can exert their function to regulate the metastasis of NSCLC through influencing the progression of epithelial‐mesenchymal transition (EMT) and the properties of cancer stem cell (CSC). But, it is necessary to do some further research to demonstrate the LncRNAs particular regulatory mechanism of inhibiting the metastasis of NSCLC and explore new drugs targeting LncRNAs.

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KCNQ1OT1 promotes melanoma growth and metastasis

Cited by 41 publications

References 25 publications

LncRNA KCNQ1OT1 Mediates Pyroptosis in Diabetic Cardiomyopathy

LncRNA KCNQ1OT1 Mediates Pyroptosis in Diabetic Cardiomyopathy

KCNQ1OT1 affects the progression of diabetic retinopathy by regulating miR‐1470 and epidermal growth factor receptor

Long non‐coding RNAs: How to regulate the metastasis of non–small‐cell lung cancer

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