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long non-coding rna A1BG-AS1 promotes tumorigenesis in breast cancer by sponging microrna-485-5p and consequently increasing expression of FLOT1 expression

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HUMAN CELL 2021年第5期34卷 1517-1531页

作者： Cai, Shibin Zhou, Yi Pan, Ying Liu, Pengpeng Yu, Kaijie Chen, Shuzheng Zhejiang Univ Lishui Hosp Dept Breast Surg Sch Med 289 Kuocang Rd Lishui 323000 Zhejiang Peoples R China

The dysregulated long non-coding rna A1BG antisense rna 1 (A1BG-AS1) has been implicated in the oncogenicity of hepatocellular carcinoma. Using reverse transcription quantitative polymerase chain reaction in this study, we detected A1BG-AS1 expression in breast cancer and elucidated the regulatory functions and exact mechanisms of A1BG-AS1 in breast cancer cells. The regulatory functions of A1BG-AS1 were examined in vitro using the Cell Counting Kit-8 assay, flow cytometric, and Transwell migration and invasion assays and in vivo through tumor xenograft experiments. In addition, we performed bioinformatics analysis, luciferase reporter assay, rna immunoprecipitation, and rescue experiments to verify the interaction among A1BG-AS1, microrna-485-5p (miR-485-5p), and flotillin-1 (FLOT1) in breast cancer. We found A1BG-AS1 to be highly expressed in breast cancer tissues and cell lines. In terms of function, depleted A1BG-AS1 markedly suppressed cell proliferation, accelerated cell apoptosis, and hindered cell migration and invasion in breast cancer. Furthermore, A1BG-AS1 interference reduced tumor growth in vivo. Mechanistic investigations confirmed that A1BG-AS1 directly interacted with miR-485-5p as a molecular sponge. We demonstrated that FLOT1 is a direct target of miR-485-5p, which could be positively regulated by A1BG-AS1 by competing for miR-485-5p. Rescue experiments clearly showed that the downregulation of miR-485-5p and upregulation of FLOT1 were capable of reversing the anticancer activities of A1BG-AS1 deficiency in terms of breast cancer cell malignancy. A1BG-AS1 acts as a miR-485-5p sponge and subsequently increases FLOT1 expression in breast cancer cells, ultimately facilitating cancer progression. Hence, the A1BG-AS1/miR-485-5p/FLOT1 pathway might offer a novel therapeutic perspective for breast cancer.

关键词： long non-coding rna Competing endogenous rnas Breast cancer Therapeutic target A1BG antisense rna 1

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long non-coding rna-mediated mechanisms independent of the rnai pathway in animals and plants

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rna BIOLOGY 2011年第3期8卷 404-414页

作者： Au, Phil Chi Khang Zhu, Qian-Hao Dennis, Elizabeth S. Wang, Ming-Bo Commonwealth Sci & Ind Res Org Plant Ind Canberra ACT Australia

Recent advances in the field of rna research have provided compelling evidence implicating long non-coding rna molecules in many diverse and substantial biological processes that include transcriptional and post-transcriptional regulation of gene expression, genomic imprinting, modulation of protein activity and subcellular localization and cellular structural maintenance. While long non-coding rnas have been most extensively studied in animal species, studies of long non-coding rna in plants begin to emerge showing some conservation of mechanisms. This review aims to provide an overview of significant and recently identified long non-coding rna-mediated mechanisms in both animal and plant species.

关键词： long non-coding rna chromatin modifications transcriptional gene regulation translational gene regulation transcription factor regulation

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long non-coding rna in glioma: novel genetic players in temozolomide resistance

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ANIMAL CELLS AND SYSTEMS 2023年第1期27卷 19-28页

作者： Roh, Jungwook Im, Mijung Kang, JiHoon Youn, BuHyun Kim, Wanyeon Korea Natl Univ Educ Dept Sci Educ Cheongju South Korea Emory Univ Sch Med Winship Canc Inst Emory Dept Hematol & Med Oncol Atlanta GA USA Pusan Natl Univ Dept Biol Sci Pusan South Korea Korea Natl Univ Educ Dept Biol Educ Cheongju South Korea Pusan Natl Univ Dept Biol Sci Busandaehak ro 63beon gil 2 Pusan 46241 South Korea Korea Natl Univ Edu Dept Biol Educ 250 Taeseongtabyeon roGangnae myeon Cheongju 28173 South Korea

Glioma is the most common primary malignant brain tumor in adults and accounts for approximately 80% of brain and central nervous system tumors. In 2021, the World Health Organization (WHO) published a new taxonomy for glioma based on its histological features and molecular alterations. Isocitrate dehydrogenase (IDH) catalyzes the decarboxylation of isocitrate, a critical metabolic reaction in energy generation in cells. Mutations in the IDH genes interrupt cell differentiation and serve as molecular biomarkers that can be used to classify gliomas. For example, the mutant IDH is widely detected in low-grade gliomas, whereas the wild type is in high-grade ones, including glioblastomas. long non-coding rnas (lncrnas) are epigenetically involved in gene expression and contribute to glioma development. To investigate the potential use of lncrnas as biomarkers, we examined lncrna dysregulation dependent on the IDH mutation status. We found that several lncrnas, namely, AL606760.2, H19, MALAT1, PVT1 and SBF2-AS1 may function as glioma risk factors, whereas AC068643.1, AC079228.1, DGCR5, FAM13A-AS1, HAR1A and WDFY3-AS2 may have protective effects. Notably, H19, MALAT1, PVT1, and SBF2-AS1 have been associated with temozolomide resistance in glioma patients. This review study suggests that targeting glioma-associated lncrnas might aid the treatment of glioma.

关键词： Isocitrate dehydrogenase long non-coding rna glioma temozolomide resistance

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long non-coding rna NEAT1 Serves as Sponge for miR-365a-3p to Promote Gastric Cancer Progression via Regulating ABCC4

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ONCOTARGETS AND THERAPY 2020年 13卷 3977-3985页

作者： Gao, Ming Liu, Liying Zhang, Dianbao Yang, Yudan Chang, Zhiwei Zhengzhou Univ Dept Oncol Affiliated Hosp 1 1 East Jianshe Rd Zhengzhou 450052 Peoples R China First Peoples Hosp Zhengzhou Dept Med Record Zhengzhou 450004 Peoples R China Henan Univ Sci & Technol Dept Oncol Affiliated Hosp 1 Luoyang 471003 Peoples R China

Introduction: long non-coding rna (lncrna) was reported to be a crucial regulator in cancer. In this work, our purpose is to explore the biological roles of nuclear paraspeckle assembly transcript 1 (NEAT1) in gastric cancer (GC). Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect NEAT1 expression in GC cells and normal cells. GC cell behaviors after NEAT1 overexpression or downregulation were analyzed by Cell Counting Kit-8 assay, colony formation assay, wound-healing assay, and flow cytometry assay. Bioinformatic tools were used to analyze the significance of NEAT1 in GC. The involvement of microrna-365a-3p (miR-365a-3p) and ATP-binding cassette subfamily C member 4 (ABCC4) in the biological roles of NEAT1 in GC progression was validated by luciferase activity reporter assay and rescue experiments. Results: We found NEAT1 increased expression in both GC tissues and cells and correlated with poorer overall survival of cancer patients. We found NEAT1 overexpression promotes, while its knockdown inhibits GC cell proliferation, colony formation, invasion, and cell cycle progression in vitro. Mechanism analyses showed that NEAT1 serves as a cerna to upregulate ABCC4 expression via sponging miR-365a-3p. Conclusion: In this study, we revealed a NEAT1/miR-365a-3p/ABCC4 triplet in GC progression, which may provide novel targeted therapy markers for GC.

关键词： long non-coding rna NEAT1 miR-365a-3p ABCC4 gastric cancer

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long non-coding rna SBF2-AS1 promotes hepatocellular carcinoma progression through regulation of miR-140-5p-TGFBR1 pathway

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2018年第4期503卷 2826-2832页

作者： Li, Yu Liu, Gang Li, Xiaojun Dong, Huiyuan Xiao, Weike Lu, Shaokang 5th Hosp PLA Dept Gen Surg Ningxia 750000 Peoples R China FuLing Cent Hosp Dept Hepatobiliary Surg Chongqing 408000 Peoples R China

A growing number of studies has suggested that long non-coding rnas (lncrnas) exert essential roles in the development and progression of hepatocellular carcinoma (HCC). However, the roles of lncrna and its molecular mechanism in HCC are largely unknown. In the present study, the functions and molecular mechanisms of a novel lncrna, SET-binding factor 2 (SBF2) antisense rna1 (SBF2-AS1), were investigated in HCC tissues and cell lines. We found that the expression levels of SBF2-AS1 were significantly up-regulated in HCC tissues and correlated with poor prognosis. SBF2-AS1 knockdown could inhibit the proliferation of HCC cells and attenuate the development of HCC tumor in vivo. Moreover, wound healing and Transwell assays revealed that down-regulation of SBF2-AS1 suppressed the migration and invasion of HCC cells by modulating epithelial-mesenchymal transition (EMT) ability. Mechanistically, we observed that SBF2-AS1 served as a competing endogenous rna (cerna) of miR-140-5p. Subsequently, transforming growth factor beta receptor 1 (TGFBR1) was certified as a direct target of miR-140-5p and enforcing SBF2-AS1 expression elevated TGFBR1 expression in HCC. Taken together, our study suggested that SBF2-AS1 modulated TGFBR1 through sponging miR-140-5p in HCC development and progression indicating that SBF2-AS1 might be further chosen as a potential anticancer therapeutic target and a promising prognostic biomarker for HCC. (C) 2018 Elsevier Inc. All rights reserved.

关键词： long non-coding rna Hepatocellular carcinoma SBF2-AS1 Progression Prognosis miR-140-5p-TGFBR1 pathway

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long non-coding rna MEG3 inhibits NSCLC cells proliferation and induces apoptosis by affecting p53 expression

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BMC CANCER 2013年第1期13卷 1-11页

作者： Lu, Kai-hua Li, Wei Liu, Xiang-hua Sun, Ming Zhang, Mei-ling Wu, Wei-qin Xie, Wei-ping Hou, Ya-yi Nanjing Med Univ Dept Oncol Affiliated Hosp 1 Nanjing Jiangsu Peoples R China Nanjing Med Univ Dept Biochem & Mol Biol Nanjing Jiangsu Peoples R China Nanjing Med Univ Dept Resp Affiliated Hosp 1 Nanjing Jiangsu Peoples R China Nanjing Univ Sch Med Immunol & Reprod Biol Lab Nanjing 210008 Jiangsu Peoples R China Nanjing Univ State Key Lab Pharmaceut Biotechnol Nanjing 210008 Jiangsu Peoples R China

Background: long non-coding rnas play an important role in tumorigenesis, hence, identification of cancer-associated lncrnas and investigation of their biological functions and molecular mechanisms are important for understanding the development and progression of cancer. Recently, the downregulation of lncrna MEG3 has been observed in various human cancers. However, its role in non-small cell lung cancer (NSCLC) is unknown. The aim of this study was to examine the expression pattern of MEG3 in NSCLC and to evaluate its biological role and clinical significance in tumor progression. Methods: Expression of MEG3 was analyzed in 44 NSCLC tissues and 7 NSCLC cell lines by qRT-PCR. Overexpression approaches were used to investigate the biological functions of MEG3 in NSCLC cells. Bisulfite sequencing was used to investigate DNA methylation on MEG3 expression. The effect of MEG3 on proliferation was evaluated by MTT and colony formation assays, and cell apoptosis was evaluated by Hoechst staining and Flow-cytometric analysis. NSCLC cells transfected with pCDNA-MEG3 were injection into nude mice to study the effect of MEG3 on tumorigenesis in vivo. Protein levels of MEG3 targets were determined by western blot analysis. Differences between groups were tested for significance using Student's t-test (two-tailed). Results: MEG3 expression was decreased in non-small cell lung cancer (NSCLC) tumor tissues compared with normal tissues, and associated with advanced pathologic stage, and tumor size. Moreover, patients with lower levels of MEG3 expression had a relatively poor prognosis. Overexpression of MEG3 decreased NSCLC cells proliferation and induced apoptosis in vitro and impeded tumorigenesis in vivo. MDM2 and p53 protein levels were affected by MEG3 over-expression in vitro. Conclusions: Our findings indicate that MEG3 is significantly down-regulated in NSCLC tissues that could be affected by DNA methylation, and regulates NSCLC cell proliferation and apoptosis, partially

关键词： long non-coding rna MEG3 NSCLC Proliferation p53

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long non-coding rna ECRAR Triggers Post-natal Myocardial Regeneration by Activating ERK1/2 Signaling

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MOLECULAR THERAPY 2019年第1期27卷 29-45页

作者： Chen, Yanmei Li, Xinzhong Li, Bing Wang, He Li, MengSha Huang, Senlin Sun, Yili Chen, Guojun Si, Xiaoyun Huang, Chixiong Liao, Wangjun Liao, Yulin Bin, Jianping Southern Med Univ Nanfang Hosp Dept Cardiol State Key Lab Organ Failure Res 1838 North Guangzhou Ave Guangzhou 510515 Guangdong Peoples R China Nanchang Univ Affiliated Hosp 3 Dept Cardiol Nanchang 330006 Jiangxi Peoples R China Southern Med Univ Nanfang Hosp Dept Oncol Guangzhou 510515 Guangdong Peoples R China

Reactivating post-natal myocardial regeneration potential may be a feasible strategy to regenerate the injured adult heart. long non-coding rnas (lncrnas) have been implicated in regulating cellular differentiation, but whether they can elicit a regenerative response in the post-natal heart remains unknown. In this study, by characterizing the lncrna transcriptome in human hearts during the fetal-to-adult transition, we found that 3,092 lncrnas were differentially expressed, and we further identified a novel upregulated fetal lncrna that we called endogenous cardiac regeneration-associated regulator (ECRAR), which promoted DNA synthesis, mitosis, and cytokinesis in post-natal day 7 and adult rat cardiomyocytes (CMs). Overexpression of ECRAR markedly stimulated myocardial regeneration and induced recovery of cardiac function after myocardial infarction (MI). Knockdown of ECRAR inhibited post-natal day 1 CM proliferation and prevented post-MI recovery. ECRAR was transcriptionally upregulated by E2F transcription factor 1 (E2F1). In addition, ECRAR directly bound to and promoted the phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2), resulting in downstream targets of cyclin D1 and cyclin E1 activation, which, in turn, activated E2F1. The E2F1-ECRAR-ERK1/2 signaling formed a positive feedback loop to drive cell cycle progression, and, therefore, it promoted CM proliferation. These findings indicated that our newly discovered ECRAR may be a valuable therapeutic target for heart failure.

关键词： long non-coding rna myocardial regeneration cell cycle ERK signaling cardiomyocyte proliferation

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long non-coding rna variability in porcine skeletal muscle

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JOUrnaL OF APPLIED GENETICS 2024年第3期65卷 565-573页

作者： Hofman, Bartlomiej Szyda, Joanna Fraszczak, Magdalena Mielczarek, Magda Wroclaw Univ Environm & Life Sci Dept Genet Biostat Grp Kozuchowska 7 PL-51631 Wroclaw Poland

Recently, numerous studies including various tissues have been carried out on long non-coding rnas (lncrnas), but still, its variability has not yet been fully understood. In this study, we characterised the inter-individual variability of lncrnas in pigs, in the context of number, length and expression. Transcriptomes collected from muscle tissue belonging to six Polish Landrace boars (PL1-PL6), including half-brothers (PL1-PL3), were investigated using bioinformatics (lncrna identification and functional analysis) and statistical (lncrna variability) methods. The number of lncrna ranged from 1289 to 3500 per animal, and the total number of common lncrnas among all boars was 232. The number, length and expression of lncrnas significantly varied between individuals, and no consistent pattern has been found between pairs of half-brothers. In detail, PL5 exhibits lower expression than the others, while PL4 has significantly higher expression than PL2-PL3 and PL5-PL6. Noteworthy, comparing the inter-individual variability of lncrna and mrna expression, they exhibited concordant patterns. The enrichment analysis for common lncrna target genes determined a variety of biological processes that play fundamental roles in cell biology, and they were mostly related to whole-body homeostasis maintenance, energy and protein synthesis as well as dynamics of multiple nucleoprotein complexes. The high variability of lncrna landscape in the porcine genome has been revealed in this study. The inter-individual differences have been found in the context of three aspects: the number, length and expression of lncrnas, which contribute to a better understanding of its complex nature.

关键词： Gene ontology, Inter-individual variability long non-coding rna Muscle tissue mrna Pigs

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long non-coding rna FOXD3-AS1 regulates the expression and secretion of IL-25 in nasal epithelial cells to inhibit Th2 type immunoreaction in allergic rhinitis

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MOLECULAR AND CELLULAR BIOCHEMISTRY 2020年第1-2期473卷 239-246页

作者： Zhang, Hao Zhu, Xinhua Liu, Xiao Wang, Yaojie Liu, Yuehui Nanchang Univ Dept Otorhinolaryngol Head & Neck Surg Affiliated Hosp 2 1 Minde Rd Nanchang 330006 Jiangxi Peoples R China

long non-coding rna FOXD3-AS1 is associated with allergic rhinitis (AR). This article aims to demystify the role of FOXD3-AS1 in AR. We compared FOXD3-AS1 expression in nasal mucosas between AR patients and healthy control. Next, nasal epithelial cells (NECs) were incubated with lipopolysaccharide or recombinant IL-25, and then the supernatant of the NECs was incubated with CD4(+)T cells. Th2 cell proportions were assessed by flow cytometry. The levels of gene and cytokines were detected by real-time quantitative PCR or enzyme linked immunosorbent assay. FOXD3-AS1 was downregulated in nasal mucosas of AR patients, whereas Th2 cell proportions and the levels of IL-25, IL-4, and IL-13 were enhanced in peripheral blood of AR patients. FOXD3-AS1 overexpression inhibited the expression and secretion of IL-25 in NECs. The levels of IL-4 and IL-13 and Th2 cell proportions in CD4(+)T cells were enhanced by recombinant IL-25, which was effectively abolished by the supernatant of FOXD3-AS1-overexpressed NECs treatment. Our study demonstrates that FOXD3-AS1 is downregulated in nasal mucosas of AR patients, and FOXD3-AS1 represses the expression and secretion IL-25 in NECs, thereby inhibiting Th2 type immunoreaction in AR. Thus, our data provide a novel target gene for AR treatment.

关键词： long non-coding rna FOXD3-AS1 IL-25 Th2 type immunoreaction Allergic rhinitis

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long non-coding rna expression profiles in neutrophils revealed potential biomarker for prediction of renal involvement in SLE patients

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RHEUMATOLOGY 2021年第4期60卷 1734-1746页

作者： Cai, Bin Cai, Jingyi Yin, Zhihua Jiang, Xiaoyue Yao, Chao Ma, Jianyang Xue, Zhixin Miao, Ping Xiao, Qingqing Cheng, Yijun Qin, Jialin Guo, Qiang Shen, Nan Ye, Zhizhong Qu, Bo Ding, Huihua Shanghai Jiao Tong Univ Renji Hosp Sch Med Shanghai Inst RheumatolDept Rheumatol Shan Dong Middle Rd Shanghai 200001 Peoples R China Shenzhen Futian Hosp Rheumat Dis Dept Rheumatol Shenzhen Peoples R China Chinese Acad Sci Inst Hlth Sci Shanghai Inst Biol Sci Lab Mol Rheumatol Shanghai Peoples R China Shanghai Jiao Tong Univ Renji Hosp China Australia Ctr Personalized Immunol Sch Med Shanghai Peoples R China Shanghai Jiao Tong Univ Renji Hosp Sch Med Dept Lab Med Shanghai Peoples R China Shanghai Jiao Tong Univ Renji Hosp Sch Med Dept Cardiol Shanghai Peoples R China Cincinnati Childrens Hosp Med Ctr Ctr Autoimmune Genom & Etiol Cincinnati OH USA Univ Cincinnati Coll Med Dept Pediat Cincinnati OH USA

Objective. The long non-coding rna plays an important role in inflammation and autoimmune diseases. The aim of this study is to screen and identify abnormally expressed lncrnas in peripheral blood neutrophils of SLE patients as novel biomarkers and to explore the relationship between lncrnas levels and clinical features, disease activity and organ damage. Methods. rna-seq technology was used to screen differentially expressed lncrnas in neutrophils from SLE patients and healthy donors. Based on the results of screening, candidate lncrna levels in neutrophils of 88 SLE patients, 35 other connective disease controls, and 78 healthy controls were qualified by real-time quantitative polymerase chain reaction. Results. Lncrna expression profiling revealed 360 up-regulated lncrnas and 224 down-regulated lncrnas in neutrophils of SLE patients when compared with healthy controls. qPCR assay validated that the expression of Lnc-FOSB-1:1 was significantly decreased in neutrophils of SLE patients when compared with other CTD patients or healthy controls. It correlated negatively with SLE Disease Activity Index 2000 (SLEDAI-2K) score (r = -0.541, P < 0.001) and IFN scores (r = -0.337, P = 0.001). More importantly, decreased Lnc-FOSB-1:1 expression was associated with lupus nephritis. Lower baseline Lnc-FOSB-1:1 level was associated with higher risk of future renal involvement (within an average of 2.6 years) in patients without renal disease at baseline (P = 0.019). Conclusion. Lncrna expression profile in neutrophils of SLE patients revealed differentially expressed lncrnas. Validation study on Lnc-FOSB-1:1 suggest that it is a potential biomarker for prediction of near future renal involvement.

关键词： systemic lupus erythematosus lupus nephritis biomarkers long non-coding rna

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