Negative regulation of lncRNA GAS5 by miR-21

Zhang, Z; Zhu, Zhengwei; Watabe, Kounosuke; Zhang, X; Bai, Chunxue; Xu, Min; Wu, Fang‐Xiang; Mo, Yuchang

doi:10.1038/cdd.2013.110

Cited by 381 publications

(353 citation statements)

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“…It has been reported that lncRNA GAS5 was negatively regulated by miR-21 in breast tumors, hepatocellular carcinoma and osteoarthritis. GAS5 was also capable of suppressing miR-21 through an lncRNA/miRNA interaction, implying a feedback loop between GAS5 and miR-21 (8,(25)(26)(27). However, in the present study, GAS5 as well as miR-21 were identified to be upregulated in the CD4 + T cells of SLE patients, which may be associated with different types of diseases and cells (8,28,29).…”

Section: Discussioncontrasting

confidence: 60%

Association of long non‑coding RNA GAS5 and miR‑21 levels in CD4+ T cells with clinical features of systemic lupus erythematosus

et al. 2017

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Abstract. The present study aimed to assess the expression of growth arrest-specific 5 (GAS5) and microRNA (miR)-21 in systemic lupus erythematosus (SLE), and attempted to explore their association with clinical features. CD4 + T cells were isolated from peripheral blood of healthy donors and SLE patients by magnetic-activated cell sorting. GAS5 and miR-21 expression levels in cluster of differentiation (CD)4 + T cells were measured by reverse-transcription quantitative polymerase chain reaction. The results revealed that GAS5 and miR-21 levels were significantly elevated in CD4 + T cells of patients with SLE compared with those in control subjects (P<0.05). Regarding clinical features, SLE patients with ulceration had higher GAS5 expression levels in CD4 + T cells than those without ulceration (P<0.05), and the expression of miR-21 was significantly higher in CD4 + T cells of SLE patients with low levels of complement component 3 (C3) than in those with normal levels of complement C3 (P<0.05).In conclusion, GAS5 and miR-21 in CD4 + T cells may serve as potential biomarkers for the diagnosis and monitoring of the progression of SLE. IntroductionSystemic lu pus erythematosus (SLE) is a multisystemic, chronic inflammatory autoimmune disease of unknown etiology. It is characterized by various pathogenic autoantibodies and immune complexes as well as damage to multiple organ systems, and the course of SLE is long followed by remission and acute attack. The prevalence varies from 31-70/100,000 individuals in China and from 20-70/100,000 individuals worldwide. It is sex-associated, occurring nine times more often in women than in men, particularly in women of child-bearing age (15-35 years) (1-3). The interaction between certain genetic and environmental factors, including chemical factors, viruses and drugs, damages normal immune tolerance and contributes to SLE. Dysfunctional T cells interact with new antigens constantly, leading to a persistent autoimmune reaction (4,5). Previous studies have confirmed that the abnormal activation and proliferation of self-reactive cluster of differentiation (CD)4 + T lymphocytes have a central role in SLE. CD4 + T cells interact with antigen-specific B cells, to make the latter ones become more effective and produce autoantibodies. In addition, CD4 + T cells produce various cytokines when they are activated, which may engender inflammatory reactions (6,7).Long non-coding RNAs (lncRNAs) are a class of non-protein-coding RNA with transcripts longer than 200 nucleotides. They have numerous important biological functions through different molecular mechanisms, and are closely associated with a variety of clinical diseases, including tumors, metabolic disease and autoimmune diseases. Growth arrest-specific 5 (GAS5), a non-coding gene that hosts a number of small nucleolar RNAs, has been suggested to have numerous important roles in apoptosis and cell growth inhibition. Previous studies have reported that human GAS5 was upregulated in osteoarthritis (OA) patients (8) and downregulated i...

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Section: Discussioncontrasting

confidence: 60%

Association of long non‑coding RNA GAS5 and miR‑21 levels in CD4+ T cells with clinical features of systemic lupus erythematosus

et al. 2017

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“…Websites reviewed in (Fritah, et al 2014 (Rehmsmeier, et al 2004) has been used to examine miRNA/lncRNA interaction (Zhou, et al 2017a) http://bibiserv.techfak.unibielefeld.de/rnahybrid/ Increased by androgens in prostate cancer cells (Salameh, et al 2015) Suppressed by ERβ PCa-specific urine biomarker (Laxman, et al 2008 Represses onco-miR-21 (Zhang, et al 2013) inhibited miR-103 in EC cells (Guo, et al 2015) inhibited activation of the AKT/mTOR pathway in PC3 PCa cells (Xue, et al 2016a) Low expression correlated with poor prognosis in thyroid cancer tissues, co-immunoprecipitates with PI3K in HEC-1B EC cells Downregulated in breast , prostate , endometrial Sun et al 2017a), and PTC (Murugan et al 2017) tumors…”

Section: Declaration Of Interest and Fundingmentioning

confidence: 99%

Non-coding RNAs: long non-coding RNAs and microRNAs in endocrine-related cancers

Klinge

2018

Endocrine-Related Cancer

100

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Abstract:The human genome is 'pervasively transcribed' leading to a complex array of noncoding RNAs (ncRNAs) that far outnumber coding mRNAs. ncRNAs have regulatory roles in transcription and post-transcriptional processes as well numerous cellular functions that remain to be fully described. Best characterized of the 'expanding universe' of ncRNAs are the ~ 22 nucleotide microRNAs (miRNAs) that base-pair to target mRNA's 3' untranslated region within the RNA-induced silencing complex (RISC) and block translation and may stimulate mRNA transcript degradation. Long non-coding RNAs (lncRNAs) are classified as >200 nucleotides in length, but range up to several kb and are heterogeneous in genomic origin and function.LncRNAs fold into structures that interact with DNA, RNA, and proteins to regulate chromatin dynamics, protein complex assembly, transcription, telomere biology, and splicing. Some lncRNAs act as sponges for miRNAs and decoys for proteins. Nuclear-encoded lncRNAs can be taken up by mitochondria and lncRNAs are transcribed from mtDNA. Both miRNAs and lncRNAs are dysregulated in endocrine cancers. This review provides an overview on the current understanding of the regulation and function of selected lncRNAs and miRNAs, and their interaction, in endocrine-related cancers: breast, prostate, endometrial, and thyroid.

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“…A total of 15 BALB/c (nu/nu) male mice (200±2.6 g; age, 3 months) from the Animal Center of Guangzhou Province (Guangdong, China) received subcutaneous injections of 2x10 6 HepG2 cells into the axillae bilaterally. The mice were housed in a pathogen-free environment at a temperature of 20-26˚C and were exposed to 12 h light/dark cycles with free access to food and water.…”

Section: Design and Construction Of A Eukaryotic Expression Vector Formentioning

confidence: 99%

“…Small ncRNAs, including the well-documented microRNAs (miRNAs or miRs), have received great attention, since they are important in cancer (5). It has been proposed that lncRNAs are involved in the epigenetic regulation of coding genes, and thus, exert a powerful effect on a number of physiological and pathological processes, including the pathogenesis of numerous human cancers (6). It has been reported that lncRNA HOX transcript antisense intergenic RNA (HOTAIR) expression is significantly higher in HCC tissues than in adjacent non-cancerous tissues (7).…”

Section: Introductionmentioning

confidence: 99%

HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma

Chen

et al. 2016

Oncology Letters

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Abstract.Evidence is rapidly accumulating that long non-coding RNAs (lncRNAs) are involved in human tumorigenesis and are dysregulated in multiple cancers, including hepatocellular carcinoma (HCC). lncRNAs can regulate essential pathways that contribute to tumor initiation and progression with tissue specificity, which suggests that lncRNAs may be valuable biomarkers and therapeutic targets. HOX transcript antisense intergenic RNA (HOTAIR) has previously been demonstrated to be an oncogene and a negative prognostic factor in a variety of cancers; however, the factors that contribute to the upregulation of HOTAIR and the interaction between HOTAIR and microRNAs (miRNAs or miRs) are largely unknown. In the present study, the expression levels of HOTAIR, forkhead box C1 (FOXC1) and miRNA-1 were examined in 50 matched pairs of HCC and HCC cells. The effects of HOTAIR on HCC cell proliferation were tested using trypan blue exclusion assay. The effect of HOTAIR on HCC growth in vivo was determined in a (nu/nu) mouse model. A computational screening of HOTAIR promoter was conducted to search for transcription factor-binding sites. FOXC1 binding to the promoter region of HOTAIR was confirmed using a chromatin immunoprecipitation assay. A search for miRNAs that had complementary base paring with HOTAIR was performed utilizing an online software program.The interaction between miR-1 and HOTAIR was examined using a luciferase reporter assay. Gain and loss of function approaches were used to determine the changes of HOTAIR or miR-1 expression. The relative levels of FOXC1 and HOTAIR expression in HCC tissues and HepG2 cells were significantly higher than those in normal liver LO2 cells and adjacent carcinoma tissues; the relative expression of miR-1 exhibited the opposite pattern. Overexpression of HOTAIR promoted HCC cell proliferation and progression of tumor xenografts. The present authors have demonstrated that FOXC1 binds to the upstream region of HOTAIR in HCC cells and that FOXC1 activates lncRNA HOTAIR expression in HCC HepG2 cells, which suggests that HOTAIR harbors a miRNA-1 binding site. The present data revealed that this binding site is vital for the regulation of miRNA-1 by HOTAIR. Furthermore, HOTAIR negatively regulated the expression of miRNA-1 in HepG2 cells. Additionally, the present study demonstrated that the oncogenic activity of HOTAIR is in part based on the negative regulation of miR-1. Taken together, these results suggest that HOTAIR is a FOXC1-activated driver of malignancy, which acts in part through the repression of miR-1. IntroductionHepatocellular carcinoma (HCC) is the third leading cause of cancer-associated mortalities, with nearly 600,000 mortalities occurring worldwide each year (1). Although resection is considered a potentially curative treatment for HCC patients, the 1-year post-operative survival rate is only 30-40% (2). Thus, it is necessary to improve our understanding of the disease-causing mechanisms and to identify specific biomarkers for HCC progression to aid in the predictio...

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Negative regulation of lncRNA GAS5 by miR-21

Cited by 381 publications

References 54 publications

Association of long non‑coding RNA GAS5 and miR‑21 levels in CD4+ T cells with clinical features of systemic lupus erythematosus

Association of long non‑coding RNA GAS5 and miR‑21 levels in CD4+ T cells with clinical features of systemic lupus erythematosus

Non-coding RNAs: long non-coding RNAs and microRNAs in endocrine-related cancers

HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma

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