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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

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ELECTRONIC JOUrnaL OF BIOTECHNOLOGY 2024年 67卷 23-33页

作者： Xie, ZhaoLian Wang, Hui Liu, LinLin Zhang, HaiQing Liu, Jing First Affiliated Hosp Affiliated Hosp 1 Dept Hepatobiliary & Pancreat Surg Ganzhou City 341000 Jiangxi Peoples R China

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 ***: 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 *** 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://***/10.1016/***.2023.10.002.(c) 2023 The Authors. Pontificia Universidad Catolica de Valparaiso. Production and hosting by Elsevier B. V. This is an open access article under the CC BY-NC-ND license (http://***/licenses/by-nc-nd/4.0/).

关键词： Antisense transcript Biomarkers Glaucoma Homeobox box 3 long non-coding rna Microrna-93-5p Neurodegenerative disease Ophthalmic testing Opposite strand Retinal ganglion cells Risk factor

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long non-coding rna SUMO1P3 promotes hepatocellular carcinoma progression through activating Wnt/β-catenin signalling pathway by targeting miR-320a

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JOUrnaL OF CELLULAR AND MOLECULAR MEDICINE 2020年第5期24卷 3108-3116页

作者： Wu, Songsong Chen, Sheng Lin, Ning Yang, Jianchuan Fujian Med Univ Shengli Clin Med Coll Fujian Prov Hosp Dept Ultrasonog Fuzhou 350001 Peoples R China

In this study, we aimed to investigate expression profile of long non-coding rna (lncrna) SUMO1P3, and its role and molecular mechanisms in the progression of hepatocellular carcinoma (HCC). The expression of SUMO1P3 in HCC tissues and cells was detected using quantitative real-time polymerase chain reaction (qRT-PCR). The chi-squared test was used to estimate the relationship between SUMO1P3 levels and clinical characteristics of HCC cases. Cellular biological behaviours were investigated using MTT, transwell assays and wound healing assay. Bioinformatics and dual-luciferase reporter assays were performed to identify potential target of SUMO1P3 in HCC. Additionally, protein analysis was carried out using Western blot. The expression of SUMO1P3 was significantly higher in HCC tissues and cells than in non-cancerous specimens and normal cells (P < .01). Moreover, its up-regulation was closely correlated with lymph node metastasis (P = .027) and TNM stage (P = .019). SUMO1P3 knockdown inhibited the proliferation, migration and invasion of HCC cells. MiR-320a was a potential target of SUMO1P3, and its expression was negatively regulated by SUMO1P3 in HCC SUMO1P3 could activate Wnt/beta-catenin pathway, which was mediated by miR-320a. Elevated expression of SUMO1P3 predicts malignant progression among HCC patients. SUMO1P3 enhances Wnt/beta-catenin pathway through sponging miR-320a, thus contributing to aggressive progression of HCC.

关键词： hepatocellular carcinoma long non-coding rna micrornas Wnt beta-catenin pathway

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long non-coding rna APTR promotes the activation of hepatic stellate cells and the progression of liver fibrosis

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2015年第4期463卷 679-685页

作者： Yu, Fujun Zheng, Jianjian Mao, Yuqing Dong, Peihong Li, Guojun Lu, Zhongqiu Guo, Chuanyong Liu, Zhanju Fan, Xiaoming Fudan Univ Dept Gastroenterol Jinshan Hosp Shanghai 201508 Peoples R China Wenzhou Med Univ Wenzhou Key Lab Surg Affiliated Hosp 1 Wenzhou 325000 Peoples R China Wenzhou Med Univ Dept Infect Dis Affiliated Hosp 1 Wenzhou 325000 Peoples R China Ningbo Yinzhou Second Hosp Dept Hepatol Ningbo 315000 Zhejiang Peoples R China Wenzhou Med Univ Dept Emergency Affiliated Hosp 1 Wenzhou 325000 Peoples R China Tongji Univ Sch Med Shanghai Peoples Hosp 10 Dept Gastroenterol Shanghai 200072 Peoples R China

In this study, we aimed at assessing a role of Alu-mediated p21 transcriptional regulator (APTR) in hepatofibrogenesis. APTR was upregulated in fibrotic liver samples and activated hepatic stellate cells (HSCs). Knockdown of APTR inhibited the activation of HSCs in vitro and mitigated the accumulation of collagen in vivo. Importantly, APTR silencing could abrogate TGF-beta(1)-induced upregulation of alpha-SMA in HSCs. In addition, inhibition of cell cycle and cell proliferation by APTR knockdown was attenuated by p21 sirna1 in primary HSCs. Finally, serum APTR levels were increased in patients with liver cirrhosis, indicating a potential biomarker for liver cirrhosis. Collectively, evidence is proposed for a new biological role of APTR in hepatofibrogenesis. (C) 2015 Elsevier Inc. All rights reserved.

关键词： Alu-mediated p21 transcriptional regulator Hepatic stellate cells Liver fibrosis p21 long non-coding rna

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long non-coding rna GAS5 is induced by interferons and plays an antitumor role in esophageal squamous cell carcinoma

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CANCER MEDICINE 2018年第7期7卷 3157-3167页

作者： Huang, Jianbing Li, Yuan Lu, Zhiliang Che, Yun Sun, Shouguo Mao, Shuangshuang Lei, Yuanyuan Zang, Ruochuan Li, Ning Sun, Nan He, Jie Chinese Acad Med Sci Canc Hosp Natl Canc Ctr Dept Thorac Surg Beijing Peoples R China Peking Union Med Coll Beijing Peoples R China

The long non-coding rna GAS5 has been reported as a tumor suppressor in many cancers. However, its functions and mechanisms remain largely unknown in esophageal squamous cell carcinoma (ESCC). In this study, we found that GAS5 was over-expressed in ESCC tissue compared with that in normal esophageal tissue in a public database. Functional studies showed that GAS5 could inhibit ESCC cell proliferation, migration and invasion in vitro. Further analysis revealed that GAS5 was regulated by interferon (IFN) responses via the JAK-STAT pathway. Moreover, as an IFN-stimulated gene (ISG), GAS5 was a positive regulator of IFN responses. The feedback loop between GAS5 and the IFN signaling pathway plays an important antitumor role in ESCC, thus providing novel potential therapeutic targets.

关键词： esophageal squamous cell carcinoma GAS5 interferons JAK-STAT pathway long non-coding rna

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long non-coding rna HEIH suppresses the expression of TP53 through enhancer of zeste homolog 2 in oesophageal squamous cell carcinoma

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JOUrnaL OF CELLULAR AND MOLECULAR MEDICINE 2020年第18期24卷 10551-10559页

作者： Ding, XinYu Qi, Chen Min, Jie Xu, ZhiFei Huang, KeNan Tang, Hua Second Mil Med Univ Dept Minimally Invas Thorac Surg Ctr Shanghai Changzheng Hosp Shanghai 200003 Peoples R China Nanjing Univ Dept Cardiothorac Surg Jinling Hosp Sch Med Nanjing Peoples R China

It is increasingly evident that the molecular and biological functions of long non-coding rnas (lncrna) are vital for understanding the molecular biology and progression of cancer. The lncrna-HEIH, a newly identified lncrna, has been demonstrated to be up-regulated in hepatocellular cancer. However, little is known about its role in oesophageal squamous cell carcinoma (ESCC). In the present study, an obvious up-regulation of lncrna-HEIH was observed in ESCC compared to the adjacent normal tissues. Meanwhile, patients with high expression of lncrna-HEIH have significantly poorer prognosis than those with low expression. We further found that lncrna-HEIH was associated with enhancer of zeste homolog 2 (EZH2) and that this association led to the repression ofTP53. These findings indicate that lncrna-HEIH may serve as a prognostic marker and a potential therapeutic target for ESCC.

关键词： lncrna-HEIH long non-coding rna oesophageal squamous cell carcinoma TP53 zeste homolog 2

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long non-coding rna-LET is a positive prognostic factor and exhibits tumor-suppressive activity in gallbladder cancer

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MOLECULAR CARCINOGENESIS 2015年第11期54卷 1397-1406页

作者： Ma, Ming-zhe Kong, Xiang Weng, Ming-zhe Zhang, Ming-di Qin, Yi-yu Gong, Wei Zhang, Wen-jie Quan, Zhi-wei Shanghai Jiao Tong Univ Xinhua Hosp Sch Med Dept Gen Surg Shanghai 200092 Peoples R China Yangzhou Univ Sch Med Taixing Peoples Hosp Dept Gen Surg Yangzhou Jiangsu Peoples R China Shanghai Jiao Tong Univ Xinhua Hosp Sch Med Dept Endocrinol Shanghai 200092 Peoples R China Wannan Med Coll Dept Pharmacol Wuhu Anhui Peoples R China

The identification of cancer-associated long non-coding rnas (lncrnas) and the investigation of their molecular and biological functions are vital for understanding the molecular biology and progression of cancer. The lncrna-LET, a newly identified lncrna, was demonstrated to be down-regulated in hepatocellular cancer. However, little is known about its role in gallbladder cancer. In the present study, an obvious down-regulation of lncrna-LET was observed in gallbladder cancer compared to their adjacent normal tissues. Meanwhile, patients with low expression of lncrna-LET have significantly poorer prognosis than those with high expression. We confirmed that hypoxia decreased lncrna-LET levels in gallbladder cancer cells. Moreover, lncrna-LET overexpression was further validated to inhibit the invasion of gallbladder cancer cells under hypoxic or normoxic conditions in vitro. We demonstrated that lncrna-LET overexpression conferred a proliferative advantage to tumor cells under hypoxic conditions. The ectopic expression of lncrna-LET led to the promotion of cell cycle arrest at G0/G1 phase and to the induction of apoptosis under hypoxic conditions. Ectopic expression of Lncrna-LET also suppressed gallbladder tumor growth in vivo. Our findings indicate that lncrna-LET may represent a prognostic marker and a potential therapeutic target for gallbladder cancer. (c) 2014 Wiley Periodicals, Inc.

关键词： gallbladder cancer lncrna-LET hypoxia prognosis long non-coding rna

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long non-coding rna MIR4435-1HG promotes cancer growth in clear cell renal cell carcinoma

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CANCER BIOMARKERS 2020年第1期29卷 39-50页

作者： Wu, Kerong Hu, Linkun Lv, Xiuyi Chen, Junfeng Yan, Zejun Jiang, Junhui Cheng, Yue Hou, Jianquan Ningbo First Hosp Ningbo Clin Res Ctr Urol Dis Dept Urol Translat Res Lab Urol Ningbo Zhejiang Peoples R China Soochow Univ Affiliated Hosp 1 Dept Urol Suzhou 215000 Jiangsu Peoples R China

BACKGROUND: long non-coding rnas (lncrnas) play important roles in cancer development, yet their roles in renal carcinoma remain unclear. OBJECTIVE: We performed this study in order to investigate the expression and roles of lncrnas in renal cell carcinoma. METHODS: In this study, we investigated the expression of lncrnas in renal cell carcinoma through microarray analysis. Quantitative real-time PCR was performed to measure the expression of lncrnas. Gain- or loss-of-function experiments were performed to investigate the roles of lncrnas in cell proliferation and apoptosis. rna pull-down and western blotting were performed to explore the underlying mechanism. RESULTS: The microarray analysis identified an upregulated lncrna MIR4435-1HG in renal carcinoma. The expression level of MIR4435-1HG was correlated with TNM stage, tumor size, and Fuhrman grade. High expression of MIR4435-1HG indicated poor prognosis. MIR4435-1HG knockdown inhibited cell proliferation, and suppressed the migrating and invasive capacity of renal carcinoma cells. rna pull-down followed by mass spectrometry revealed an interaction between MIR4435-1HG and pyruvate carboxylase, which was later corroborated by western blotting. CONCLUSIONS: MIR4435-1HG plays a critical role in the oncogenesis of renal cell carcinoma and may serve as a potential biomarker for renal cell carcinoma.

关键词： long non-coding rna MIR4435-1HG pyruvate carboxylase renal cell carcinoma tumorigenesis

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long non-coding rna CASC2 serves as a cerna of microrna-21 to promote PDCD4 expression in oral squamous cell carcinoma

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ONCOTARGETS AND THERAPY 2019年 12卷 3377-3385页

作者： Pan, Lina Chen, Hui Bai, Yang Wang, Qibao Chen, Liang Jinan Stomatol Hosp Shungeng Campus Jinan 250001 Shandong Peoples R China Jinan Stomatol Hosp Dept Endodont Jinan 250001 Shandong Peoples R China

Background: Oral squamous cell carcinoma (OSCC) is a common oral disease with high morbidity and mortality. Recently, long non-coding rnas (lncrnas) were identified as critical regulators in OSCC tumorigenesis. The present study aimed to work out the functions and the possible molecular mechanisms of lncrna CASC2 in human OSCC. Methods: The expression levels of CASC2 in clinical OSCC tissue samples and cultured OSCC cell lines were detected by RT-qPCR analysis. MTT assay was performed to detect the proliferation ability of OSCC cells, whereas the apoptosis rate and cell cycle distribution of OSCC cells were determined by flow cytometric analysis. The expression levels of relevant proteins were detected by Western blot assay. Dual-luciferase reporter assay was performed to validate the predicted relationship between CASC2, miR-21 amd PDCD4. The role of CASC2 in OSCC tumorigenesis in vivo was evaluated using a nude mouse tumor model. Results: The results demonstrated that CASC2 was significantly downregulated in clinical OSCC tissue samples and cultured OSCC cell lines. Low CASC2 expression was closely correlated with adverse clinicopathological characteristics of OSCC patients. Functionally, overexpression of CASC2 remarkably inhibited cell proliferation partly through inducing cell cycle arrest and cell apoptosis. Furthermore, bioinformatics analysis and dual-luciferase reporter assay showed that CASC2 might act as a competing endogenous rna of miR-21 to promote the expression of PDCD4. Rescue experiments also showed that miR-21 blocked the tumor-suppressive role that CASC2 exerted in OSCC cells. Finally, in vivo study indicated that overexpression of CASC2 restrained OSCC tumor growth in volume and weight. Conclusion: In conclusion, these findings indicate that CASC2/miR-21/PDCD4 axis might be a potential regulator of OSCC tumorigenesis, and shed new light on lncrna-directed diagnostics and therapeutics in OSCC.

关键词： oral squamous cell carcinoma long non-coding rna CASC2 microrna-21 PDCD4

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long non-coding rna ANRIL regulates inflammatory responses as a novel component of NF-κB pathway

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rna BIOLOGY 2016年第1期13卷 98-108页

作者： Zhou, Xiao Han, Xiaorui Wittfeldt, Ann Sun, Jingzhi Liu, Chujun Wang, Xiaoxia Gan, Li-Ming Cao, Huiqing Liang, Zicai Peking Univ Inst Mol Med Lab Nucl Acid Technol Beijing 100871 Peoples R China Univ Gothenburg Sahlgrenska Acad Inst Med Dept Mol & Clin Med Gothenburg Sweden Jining Med Univ Affiliated Hosp Dept Cardiol Jining 272000 Peoples R China Peking Univ Inst Mol Med Beijing Key Lab Cardiometabol Mol Med Beijing 100871 Peoples R China AstraZeneca R&D Molndal Sweden

Antisense noncoding rna in the INK4 Locus (ANRIL) is the prime candidate gene at Chr9p21, the well-defined genetic risk locus associated with multiple human diseases including coronary artery disease (CAD), while little is known regarding its role in the pathological processes. Endothelial dysfunction triggers atherosclerotic processes that are causatively linked to CAD. To evaluate the function of ANRIL in human endothelial cells (ECs), we examined ANRIL expression under pathological stimuli and found ANRIL was markedly induced by pro-inflammatory factors. Loss-of-function and chromatin immunoprecipitation approaches revealed that NF-kappa B mediates TNF-alpha induced ANRIL expression. rna sequencing revealed that ANRIL silencing dysregulated expression of inflammatory genes including IL6 and IL8 under TNF-alpha treatment. We explored the regulatory mechanism of ANRIL on IL6/8 and found that Yin Yang 1 (YY1), an ANRIL binding transcriptional factor revealed by rna immunoprecipitation, was required for IL6/8 expression under TNF-alpha treatment. YY1 was enriched at promoter loci of IL6/8 and ANRIL silencing impaired the enrichment, indicating a cooperation between ANRIL and YY1 in the regulation of inflammatory genes. For the first time, we establish the connection between ANRIL and NF-kappa B pathway and show that ANRIL regulates inflammatory responses through binding with YY1. The newly identified TNF-alpha-NF-kappa B-ANRIL/YY1-IL6/8 pathway enhances understanding of the etiology of CAD and provides potential therapeutic target for treatment of CAD.

关键词： long non-coding rna coronary artery disease YY1 inflammation NF-kappa B ANRIL

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long non-coding rna lnc_3712 impedes nuclear reprogramming via repressing Kdm5b

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MOLECULAR THERAPY-NUCLEIC ACIDS 2021年 24卷 54-66页

作者： Deng, Mingtian Wan, Yongjie Chen, Baobao Dai, Xiangpeng Liu, Zifei Yang, Yingnan Cai, Yu Zhang, Yanli Wang, Feng Nanjing Agr Univ Coll Anim Sci & Technol Jiangsu Livestock Embryo Engn Lab Nanjing 210095 Peoples R China Nanjing Agr Univ Coll Anim Sci & Technol Nanjing 210095 Peoples R China Jilin Univ First Hosp Minist Educ Key Lab Organ Regenerat & Transplantat Changchun 130021 Jilin Peoples R China

long non-coding rnas (lncrnas) are involved in shaping chromosome conformation and regulation of preimplantation development. However, the role of lncrna during somatic cell nuclear transfer (SCNT) reprogramming remains largely unknown. In the present study, we identified 114 upregulated lncrnas in the 8-cell SCNT embryos as candidate key molecules involved in nuclear reprogramming in goat. We found that H3K4me3 was an epigenetic barrier in goat nuclear reprogramming that and injection of Kdm5b mrna greatly improved SCNT embryos development through removal of H3K4me3. We further reported that knockdown of lnc_3712 increased the expression of Kdm5b, which led to H3K4me3 demethylation. Of note, the development of goat SCNT embryos was improved when lnc_3712 was knocked down, whereas the blastocyst rate showed no difference in lnc_3712 and Kdm5b double knockdown SCNT embryos compared with the negative control SCNT embryos. Specifically, in lnc_3712 knockdown SCNT embryos, partial of the transcriptional activity and the expression of critical embryonic genes (Wee1, Ctsb, and Ybx1) were similar with that of in vitro fertilization embryos. Therefore, our results elucidate the critical role of lnc_3712 in regulating the development of goat SCNT embryos via repressing Kdm5b, which advances our current understanding of the role of lncrnas during nuclear reprogramming.

关键词： somatic cell nuclear transfer reprogramming long non-coding rna Kdm5b H3K4me3 goat

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