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long non-coding rna H19 promotes TDRG1 expression and cisplatin resistance by sequestering mirna-106b-5p in seminoma

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CANCER MEDICINE 2018年第12期7卷 6247-6257页

作者： Wei, Jingchao Gan, Yu Peng, Dongyi Jiang, Xianzhen Kitazawa, Riko Xiang, Yali Dai, Yingbo Tang, Yuxin Yang, Jianfu Cent South Univ Dept Urol Xiangya Hosp 3 Changsha Hunan Peoples R China Cent South Univ Dept Urol Xiangya Hosp Changsha Hunan Peoples R China Ehime Univ Hosp Dept Diagnost Pathol Toon Japan Cent South Univ Dept Hlth Management Ctr Xiangya Hosp 3 Changsha Hunan Peoples R China Sun Yat Sen Univ Dept Urol Affiliated Hosp 5 Zhuhai Peoples R China

The role of TDRG1 in tumorigenesis and the progression of seminoma, as well as its role in regulating chemosensitivity of seminoma to cisplatin through the PI3K/Akt/mTOR signaling pathway, has been previously defined. However, the detailed mechanism underlying TDRG1 expression and concomitant chemoresistance conditions are unknown. Furthermore, it has been reported that non-protein-coding rnas play an important role in a variety of vital processes including cellular chemosensitivity. However, the role of non-protein-coding rnas in regulating the chemosensitivity of seminoma remains unknown. In this study, using microarray analysis, we found that long non-coding rna H19 was upregulated while mirna-106b-5p was downregulated in an established cisplatin-resistant TCam-2 cell line. Moreover, H19 acts as a mirna-106b-5p sponge and thus impairs the function of mirna-106b-5p on its target gene, TDRG1. Based on these findings, we propose that H19 promotes the expression of TDRG1 by sequestering mirna-106b-5p and uses this mechanism to facilitate cell survival in cisplatin-based chemotherapeutic conditions. These findings elucidate the mechanisms, at least partially, applied to deregulate TDRG1 and cisplatin sensitivity, and may provide new therapeutic possibilities for chemoresistant seminoma.

关键词： chemotherapy drug resistance long non-coding rna microrna seminoma

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long non-coding rna NORAD induces cell proliferation and migration in prostate cancer

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JOUrnaL OF INTErnaTIONAL MEDICAL RESEARCH 2019年第8期47卷 3898-3904页

作者： Zhang, Haiyan Guo, Haixiang Kunming Med Univ Affiliated Hosp 2 Dept Urol Kunming 650101 Yunnan Peoples R China

Objectives Prostate cancer (PCA) is the deadliest urological disease affecting men worldwide. long noncoding rna activated by DNA damage (NORAD) levels are increased in many cancer types, and induce cancer cell progression. However, little is known about the biological functions of NORAD in PCA. Methods In this work, the roles of NORAD in cell proliferation, migration, and apoptosis were examined by Cell Counting Kit-8, scratch wound, and annexin V-fluorescein isothiocyanate/propidium iodide staining assays, respectively, in PCA cell lines. Knockdown of NORAD was achieved by small interfering (si)rna in PCA cell lines, and quantitative real-time PCR was used to detect the expression of NORAD. Results Cell proliferation and migration rates were significantly lower in the siNORAD group than in the wild-type group, while the apoptosis level was significantly higher in the siNORAD group compared with the wild-type group. Conclusions These results suggest that NORAD promotes the proliferation and migration of PCA cells and inhibits their apoptosis.

关键词： NORAD prostate cancer proliferation migration long non-coding rna apoptosis

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long non-coding rna-based glycolysis-targeted cancer therapy: feasibility, progression and limitations

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MOLECULAR BIOLOGY REPORTS 2021年第3期48卷 2713-2727页

作者： Liu, Rui Wang, Xiaman Shen, Ying He, Aili Xi An Jiao Tong Univ Affiliated Hosp 2 Dept Hematol 1575th West Rd Xian 710004 Shaanxi Peoples R China Xi An Jiao Tong Univ Affiliated Hosp 2 Natl Local Joint Engn Res Ctr Biodiagnost & Bioth Xian 710004 Shaanxi Peoples R China

Metabolism reprogramming is one of the hallmarks of cancer cells, especially glucose metabolism, to promote their proliferation, metastasis and drug resistance. Cancer cells tend to depend on glycolysis for glucose utilization rather than oxidative phosphorylation, which is called the Warburg effect. Genome instability of oncogenes and tumor-inhibiting factors is the culprits for this anomalous glycolytic fueling, which results in dysregulating metabolism-related enzymes and metabolic signaling pathways. It has been extensively demonstrated that protein-coding genes are involved in this process;therefore, glycolysis-targeted therapy has been widely used in anti-tumor combined therapy via small molecular inhibitors of key enzymes and regulatory molecular. The long non-coding rna, which is a large class of regulatory rna with longer than 200 nucleotides, is the novel and significant regulator of various biological processes, including metabolic reprogramming. rna interference and synthetic antisense oligonucleotide for rna reduction have developed rapidly these years, which presents potent anti-tumor effects both in vitro and in vivo. However, lncrna-based glycolysis-targeted cancer therapy, as the highly specific and less toxic approach, is still under the preclinical phase. In this review, we highlight the role of lncrna in glucose metabolism and dissect the feasibility and limitations of this clinical development, which may provide potential targets for cancer therapy.

关键词： long non-coding rna Warburg effect Glucose metabolism Small molecular inhibitors rna inference Antisense oligonucleotide

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Basic Study long non-coding rna TP73-AS1 promotes pancreatic cancer growth and metastasis through mirna-128-3p/GOLM1 axis

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World Journal of Gastroenterology 2021年第17期27卷 1993-2014页

作者： Bin Wang Xing Sun Ke-Jian Huang Li-Sheng Zhou Zheng-Jun Qiu Department of General Surgery Shanghai General HospitalShanghai Jiao Tong University School of MedicineShanghai 200080China

BACKGROUND Previous studies have suggested that long non-coding rnas(lncrna)TP73-AS1 is significantly upregulated in several ***,the biological role and clinical significance of TP73-AS1 in pancreatic cancer(PC)remain *** To investigate the role of TP73-AS1 in the growth and metastasis of *** The expression of lncrna TP73-AS1,miR-128-3p,and GOLM1 in PC tissues and cells was detected by quantitative real-time polymerase chain *** bioinformatics prediction software ENCORI was used to predict the putative binding sites of *** regulatory roles of TP73-AS1 and miR-128-3p in cell proliferation,migration,and invasion abilities were verified by Cell Counting Kit-8,wound-healing,and transwell assays,as well as flow cytometry and Western blot *** interactions among TP73-AS1,miR-128-3p,and GOLM1 were explored by bioinformatics prediction,luciferase assay,and Western *** The expression of TP73-AS1 and mirna-128-3p was dysregulated in PC tissues and *** TP73-AS1 expression was correlated with a poor ***73-AS1 silencing inhibited PC cell proliferation,migration,and invasion in vitro as well as suppressed tumor growth in ***,TP73-AS1 was validated to promote PC progression through GOLM1 upregulation by competitively binding to *** Our results demonstrated that TP73-AS1 promotes PC progression by regulating the miR-128-3p/GOLM1 axis,which might provide a potential treatment strategy for patients with PC.

关键词： Pancreatic cancer long non-coding rna TP73-AS1 miR-128-3p GOLM1

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long non-coding rna H19, a novel therapeutic target for pancreatic cancer

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MOLECULAR MEDICINE 2020年第1期26卷 30-30页

作者： Wang, Jing Zhao, Lei Shang, Kun Liu, Fang Che, Juanjuan Li, Huihui Cao, Bangwei Capital Med Univ Dept Oncol Beijing Friendship Hosp 95 Yong An Rd Beijing Xicheng Distric Peoples R China Yale Sch Med New Haven CT USA Capital Med Univ Dept Cardiol Chaoyang Hosp Beijing Chaoyang Distri Peoples R China

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with high mortality, which threats peoples' health. Unfortunately, the pathogenesis of PDAC remains unclear. Recent studies have indicated that long non-coding rnas (lncrnas) can regulate the development and progression of malignant tumors through varying mechanisms. Lncrna H19 has a unique expression profile and can act as a sponger of specific mirnas to regulate the pathogenic process of many diseases, including PDAC and several other types of cancers. Here, we review the research approaches to understanding the regulatory role of H19 and potential mechanisms in the progression of PDAC and other types of cancers and diseases. These studies suggest that H19 may be a novel therapeutic target for PDAC and our findings may open new revenues for scientific researches and development of valuable therapies for these diseases in the future.

关键词： long non-coding rna H19 pancreatic ductal adenocarcinoma Proliferation Therapeutic target

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long non-coding rna: a versatile regulator of the nuclear factor-B signalling circuit

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IMMUNOLOGY 2017年第4期150卷 379-388页

作者： Mao, Xiaohua Su, Zhenyi Mookhtiar, Adnan K. Southeast Univ Dept Biochem Key Lab Minist Educ Dev Genes & Human Dis Sch Med Nanjing Jiangsu Peoples R China Harvard Med Sch Dept Cell Biol Boston MA USA

The nuclear factor-B (NF-B) family of transcription factors play an essential role for the regulation of inflammatory responses, immune function and malignant transformation. Aberrant activity of this signalling pathway may lead to inflammation, autoimmune diseases and oncogenesis. Over the last two decades great progress has been made in the understanding of NF-B activation and how the response is counteracted for maintaining tissue homeostasis. Therapeutic targeting of this pathway has largely remained ineffective due to the widespread role of this vital pathway and the lack of specificity of the therapies currently available. Besides regulatory proteins and micrornas, long non-coding rna (lncrna) is emerging as another critical layer of the intricate modulatory architecture for the control of the NF-B signalling circuit. In this paper we focus on recent progress concerning lncrna-mediated modulation of the NF-B pathway, and evaluate the potential therapeutic uses and challenges of using lncrnas that regulate NF-B activity.

关键词： cancer inflammation long non-coding rna nuclear factor-B signalling regulation

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long non-coding rna ASMTL-AS1 deteriorates the oncogenicity of osteosarcoma by decoying microrna-342-3p and consequently raising ADAM9 expression

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2021年 579卷 89-96页

作者： Hou, Chengcai Sun, Fei Sun, Mingyue Zaozhuang Municipal Hosp Dept Hand Foot & Ankle Surg Zaozhuang 277100 Shandong Peoples R China Zaozhuang Vocat Coll Med Coll Zaozhuang 277800 Shandong Peoples R China Zaozhuang Municipal Hosp Dept Traumat Orthoped 41 Longtou Middle Rd Zaozhuang 277100 Shandong Peoples R China

Background: Till now, little is known regarding expression pattern and specific roles of lncrna ASMTL antisense rna 1 (ASMTL-AS1) in osteosarcoma (OS). Therefore, our current research measured the expression of ASMTL-AS1 in OS, unveiled the roles of ASMTL-AS1 in the modulation of malignant characteristics of OS, and identified the downstream mechanism. Methods: The regulatory actions of ASMTL-AS1 ablation in OS cells were explored utilizing loss-of function experiments. Mechanistic studies were implemented utilizing bioinformatics analysis, luciferase reporter assay, rna immunoprecipitation and rescue experiments. Results: ASMTL-AS1 expression in OS was elevated in both TCGA database and our own cohort. Interfering with ASMTL-AS1 restricted cell proliferation, migration and invasion while increasing cell apoptosis in vitro. Additionally, silencing ASMTL-AS1 blocked tumour growth in vivo. Mechanistically, ASMTL-AS1 could act as a competing endogenous rna for microrna-342-3p (miR-342-3p) and inhibit its activity in OS cells, consequently causing an increase in ADAM metallopeptidase domain 9 (ADAM9) levels. Furthermore, inhibiting miR-342-3p or upregulating ADAM9 abated silenced ASMTL-AS1induced antitumour activity in OS cells. Conclusion: ASMTL-AS1 aggravated OS progression by regulating the miR-342-3p/ADAM9 axis. (c) 2021 Elsevier Inc. All rights reserved.

关键词： long non-coding rna SMTL antisense rna 1 OS therapy Therapeutic target

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long non-coding rna cardiac hypertrophy-associated regulator governs cardiac hypertrophy via regulating miR-20b and the downstream PTEN/AKT pathway

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JOUrnaL OF CELLULAR AND MOLECULAR MEDICINE 2019年第11期23卷 7685-7698页

作者： Zhang, Mingyu Jiang, Yuan Guo, Xiaofei Zhang, Bowen Wu, Jiangjiao Sun, Jiabin Liang, Haihai Shan, Hongli Zhang, Yong Liu, Jiaqi Wang, Ying Wang, Lu Zhang, Rong Yang, Baofeng Xu, Chaoqian Harbin Med Univ Key Lab Cardiovasc Med Res State Prov Key Labs Biomed Pharmaceut China Coll PharmMinist EducDept Pharmacol Xuefu Rd 194 Harbin 150081 Heilongjiang Peoples R China Harbin Med Univ Affiliated Hosp 2 Dept Pharm Harbin Heilongjiang Peoples R China Mudanjiang Med Univ Univ Alliance Sino Russian Med Univ Ctr Chron Dis & Drug Res Mudanjiang Med Mudanjiang 157011 Peoples R China Harbin Med Univ Hosp 4 Dept Urol Harbin Heilongjiang Peoples R China

Pathological cardiac hypertrophy (CH) is a key factor leading to heart failure and ultimately sudden death. long non-coding rnas (lncrnas) are emerging as a new player in gene regulation relevant to a wide spectrum of human disease including cardiac disorders. Here, we characterize the role of a specific lncrna named cardiac hypertrophy-associated regulator (CHAR) in CH and delineate the underlying signalling pathway. CHAR was found markedly down-regulated in both in vivo mouse model of cardiac hypertrophy induced by pressure overload and in vitro cellular model of cardiomyocyte hypertrophy induced by angiotensin II (AngII) insult. CHAR down-regulation alone was sufficient to induce hypertrophic phenotypes in healthy mice and neonatal rat ventricular cells (NRVCs). Overexpression of CHAR reduced the hypertrophic responses. CHAR was found to act as a competitive endogenous rna (cerna) to down-regulate miR-20b that we established as a pro-hypertrophic mirna. We experimentally established phosphatase and tensin homolog (PTEN), an anti-hypertrophic signalling molecule, as a target gene for miR-20b. We found that miR-20b induced CH by directly repressing PTEN expression and indirectly increasing AKT activity. Moreover, CHAR overexpression mitigated the repression of PTEN and activation of AKT by miR-20b, and as such, it abrogated the deleterious effects of miR-20b on CH. Collectively, this study characterized a new lncrna CHAR and unravelled a new pro-hypertrophic signalling pathway: lncrna-CHAR/miR-20b/PTEN/AKT. The findings therefore should improve our understanding of the cellular functionality and pathophysiological role of lncrnas in the heart.

关键词： cardiac hypertrophy cardiac hypertrophy-associated regulator long non-coding rna miR-20b phosphatase and tensin homolog

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long non-coding rna MALAT1 expression in patients with gestational diabetes mellitus

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INTErnaTIONAL JOUrnaL OF GYNECOLOGY & OBSTETRICS 2018年第2期140卷 164-169页

作者： Zhang, Yisheng Wu, Hangyu Wang, Fuyan Ye, Mei Zhu, Hong Bu, Shizhong Ningbo Univ Li Huili Eastern Hosp Ningbo Med Ctr Dept Gynaecol & Obstet Ningbo Zhejiang Peoples R China Ningbo Univ Sch Med Diabet Res Ctr Ningbo Zhejiang Peoples R China Ningbo Univ Affiliated Hosp Dept Obstet Ningbo Zhejiang Peoples R China

Objective: To monitor the expression of long non-coding rnas (lncrnas) and changes in metabolic profiles among patients with gestational diabetes mellitus (GDM). Methods: A retrospective case-control study was conducted using data for women treated at a hospital in China between October 8, 2014, and April 15, 2015. Patients diagnosed with GDM using an oral glucose tolerance test at 24-28weeks of pregnancy (n=50) were included. The control group comprised pregnant women without GDM (n=47). Serum levels of lncrna MALAT1, lncrna p21, and lncrna H19 were assessed using the reverse transcription polymerase chain reaction. Plasma glucose and lipid levels were assessed biochemically. Results: The expression level of lncrna MALAT1 was higher among the cases than the controls (P=0.007). Expression of Incrna MALAT1 among the patients with GDM correlated with both lncrna p21 (r=0.333, P=0.018) and lncrna H19 (r=0.314, P=0.030). Levels of triglycerides and total cholesterol differed between the control group and patients with GDM (3.6 +/- 2.6mmol/L vs 3.8 +/- 1.5mmol/L and 6.54 +/- 1.30mmol/L vs 7.40 +/- 0.90mmol/L, respectively;P<0.05). The area under the receiver operating characteristic curve was 0.654 (95% confidence interval 0.543-0.768, P<0.001). Conclusion: Expression of lncrna MALAT1 could offer a novel biomarker to predictGDM.

关键词： Gestational diabetes mellitus Lipid metabolism Lncrna H19 Lncrna MALAT1 Lncrna p21 long non-coding rna

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long non-coding rna NRON is downregulated in HCC and suppresses tumour cell proliferation and metastasis

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BIOMEDICINE & PHARMACOTHERAPY 2018年 104卷 102-109页

作者： Yao, Zhicheng Xiong, Zhiyong Li, Ruixi Liang, Hao Jia, Changchang Deng, Meihai Sun Yat Sen Univ Affiliated Hosp 3 Dept Gen Surg Guangzhou 510000 Guangdong Peoples R China Sun Yat Sen Univ Affiliated Hosp 3 Dept Hepatobiliary Surg Guangzhou 510000 Guangdong Peoples R China Sun Yat Sen Univ Affiliated Hosp 3 Dept Cell Gene Therapy Translat Med Res Ctr Guangzhou 510000 Guangdong Peoples R China

Dysregulation of long non-coding rnas is a newly identified mechanism for tumour progression. Previous studies have suggested that the nuclear factor of activated T cells (NFAT) gene plays a very important role in cancer growth and metastasis. However, lncNRON is a newly identified repressor of NFAT, and its function is largely unknown, especially in hepatocellular carcinoma (HCC). Therefore, the expression levels of lncNRON in 215 pairs of HCC tissue were evaluated by qRT-PCR, and its relationship to clinicopathological parameters, recurrence, and survival was analysed. Furthermore, stably overexpressing lncNRON cell lines were constructed and evaluated for cell phenotype. Finally, we detected epithelial-to-mesenchymal transition (EMT) proteins to determine the underlying mechanism involved in lncNRON function. We observed that lncNRON was downregulated in HCC tumour tissues;low lncNRON expression was associated with poor tumour differentiation and the presence of vascular tumour thrombus, which tended to result in poor clinical outcomes, as demonstrated by the recurrence rate and survival curves. Functional analysis showed that lncNRON overexpression impaired colony formation and cell viability and inhibited cell migration and invasion. A study using tumour-bearing mice showed that lncNRON markedly limited tumour growth and lung metastasis in vivo. Importantly, western blot analysis revealed that the expression of the EMT-related epithelial marker, E-cadherin, increased, whereas the expression of mesenchymal markers N-cadherin, snail, and vimentin was attenuated by lncNRON overexpression in HCC cells. Therefore, lower lncNRON expression indicates a poorer clinical outcome in HCC. LncNRON overexpression can suppress HCC growth and metastasis via inhibiting the EMT, and lncNRON may function as a new HCC prognostic marker.

关键词： long non-coding rna NRON Nuclear factor of activated T cells Hepatocellular carcinoma Metastasis

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