ZhaoLian Xie, Hui Wang, LinLin Liu, HaiQing Zhang, Jing Liu
{"title":"长链非编码RNA KCNQ1对链/反义转录物1是青光眼的潜在生物标志物，通过microRNA-93-5p/Homeobox box 3轴加速青光眼的进展","authors":"ZhaoLian Xie, Hui Wang, LinLin Liu, HaiQing Zhang, Jing Liu","doi":"10.1016/j.ejbt.2023.10.002","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Glaucoma is marked by retinal neuron death in the ganglion cell layer, leading to irreversible vision loss. Aberrant long non-coding RNA (lncRNA) expression is associated with glaucoma. The study was to explore the latent molecular mechanism of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in N-methyl-D-aspartate (NMDA)-stimulated glaucoma.</p></div><div><h3>Results</h3><p>The data demonstrated that KCNQ1OT1 expression was elevated in glaucoma patients, serving as a diagnostic biomarker of glaucoma. Rats injected with NMDA developed visual loss and retinopathy and expressed high KCNQ1OT1. After treating retinal ganglion cells (RGCs) with NMDA, cell proliferation was suppressed and apoptosis was augmented. Silenced KCNQ1OT1 or HOXB3 or elevated miR-93-5p alleviated NMDA-induced suppression of RGC growth. KCNQ1OT1 mediated miR-93-5p expression by targeting homeobox box 3 (HOXB3). The protection of silenced KCNQ1OT1 in NMDA-treated RGCs was turned around by elevated HOXB3.</p></div><div><h3>Conclusions</h3><p>Overall, KCNQ1OT1 accelerates glaucoma progression via miR-93-5p/HOXB3 axis.</p><p><strong>How to cite:</strong> Xie ZL, Wang H, Liu LL, et al. Long non-coding RNA KCNQ1 opposite strand/antisense transcript 1, a potential biomarker for glaucoma, accelerates glaucoma progression via microRNA-93-5p/Homeobox box 3 axis. Electron J Biotechnol 2024;67 . <span>https://doi.org/10.1016/j.ejbt.2023.10.002</span><svg><path></path></svg>.</p></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"67 ","pages":"Pages 23-33"},"PeriodicalIF":2.3000,"publicationDate":"2023-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0717345823000349/pdfft?md5=2eb492a58f21d7b63cf1e0f5268a9b4c&pid=1-s2.0-S0717345823000349-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Long non-coding RNA KCNQ1 opposite strand/antisense transcript 1, a potential biomarker for glaucoma, accelerates glaucoma progression via microRNA-93-5p/Homeobox box 3 axis\",\"authors\":\"ZhaoLian Xie, Hui Wang, LinLin Liu, HaiQing Zhang, Jing Liu\",\"doi\":\"10.1016/j.ejbt.2023.10.002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><p>Glaucoma is marked by retinal neuron death in the ganglion cell layer, leading to irreversible vision loss. Aberrant long non-coding RNA (lncRNA) expression is associated with glaucoma. The study was to explore the latent molecular mechanism of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in N-methyl-D-aspartate (NMDA)-stimulated glaucoma.</p></div><div><h3>Results</h3><p>The data demonstrated that KCNQ1OT1 expression was elevated in glaucoma patients, serving as a diagnostic biomarker of glaucoma. Rats injected with NMDA developed visual loss and retinopathy and expressed high KCNQ1OT1. After treating retinal ganglion cells (RGCs) with NMDA, cell proliferation was suppressed and apoptosis was augmented. Silenced KCNQ1OT1 or HOXB3 or elevated miR-93-5p alleviated NMDA-induced suppression of RGC growth. KCNQ1OT1 mediated miR-93-5p expression by targeting homeobox box 3 (HOXB3). The protection of silenced KCNQ1OT1 in NMDA-treated RGCs was turned around by elevated HOXB3.</p></div><div><h3>Conclusions</h3><p>Overall, KCNQ1OT1 accelerates glaucoma progression via miR-93-5p/HOXB3 axis.</p><p><strong>How to cite:</strong> Xie ZL, Wang H, Liu LL, et al. Long non-coding RNA KCNQ1 opposite strand/antisense transcript 1, a potential biomarker for glaucoma, accelerates glaucoma progression via microRNA-93-5p/Homeobox box 3 axis. 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Long non-coding RNA KCNQ1 opposite strand/antisense transcript 1, a potential biomarker for glaucoma, accelerates glaucoma progression via microRNA-93-5p/Homeobox box 3 axis
Background
Glaucoma is marked by retinal neuron death in the ganglion cell layer, leading to irreversible vision loss. Aberrant long non-coding RNA (lncRNA) expression is associated with glaucoma. The study was to explore the latent molecular mechanism of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in N-methyl-D-aspartate (NMDA)-stimulated glaucoma.
Results
The data demonstrated that KCNQ1OT1 expression was elevated in glaucoma patients, serving as a diagnostic biomarker of glaucoma. Rats injected with NMDA developed visual loss and retinopathy and expressed high KCNQ1OT1. After treating retinal ganglion cells (RGCs) with NMDA, cell proliferation was suppressed and apoptosis was augmented. Silenced KCNQ1OT1 or HOXB3 or elevated miR-93-5p alleviated NMDA-induced suppression of RGC growth. KCNQ1OT1 mediated miR-93-5p expression by targeting homeobox box 3 (HOXB3). The protection of silenced KCNQ1OT1 in NMDA-treated RGCs was turned around by elevated HOXB3.
Conclusions
Overall, KCNQ1OT1 accelerates glaucoma progression via miR-93-5p/HOXB3 axis.
How to cite: Xie ZL, Wang H, Liu LL, et al. Long non-coding RNA KCNQ1 opposite strand/antisense transcript 1, a potential biomarker for glaucoma, accelerates glaucoma progression via microRNA-93-5p/Homeobox box 3 axis. Electron J Biotechnol 2024;67 . https://doi.org/10.1016/j.ejbt.2023.10.002.
期刊介绍：
Electronic Journal of Biotechnology is an international scientific electronic journal, which publishes papers from all areas related to Biotechnology. It covers from molecular biology and the chemistry of biological processes to aquatic and earth environmental aspects, computational applications, policy and ethical issues directly related to Biotechnology.
The journal provides an effective way to publish research and review articles and short communications, video material, animation sequences and 3D are also accepted to support and enhance articles. The articles will be examined by a scientific committee and anonymous evaluators and published every two months in HTML and PDF formats (January 15th , March 15th, May 15th, July 15th, September 15th, November 15th).
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