miR‐185 affected the EMT, cell viability, and proliferation via DNMT1/MEG3 pathway in TGF‐β1‐induced renal fibrosis DOI
Rong Xue, Yingping Li, Xiaoli Li

et al.

Cell Biology International, Journal Year: 2018, Volume and Issue: 43(10), P. 1152 - 1162

Published: Aug. 10, 2018

Abstract Kidney fibrosis is usually the final manifestation of a wide variety renal diseases. Recent years, research reported that long non‐coding RNAs (lncRNAs) played important roles in human However, role and underlying mechanisms lncRNAs kidney were complicated largely unclear. In our study, we constructed cell model HK2 cells using transforming growth factor β1 (TGF‐β1) found lncRNA maternally expressed gene 3 (MEG3) was downregulated TGF‐β1‐induced fibrosis. We then overexpressed MEG3 inhibited promotion epithelial–mesenchymal transition, viability, proliferation. Furthermore, demonstrated DNA methyltransferases 1 (DNMT1) regulated expression by altering CpGs methylation level promoter addition, further revealed miR‐185 could regulate DNMT1 thus, modulate Ultimately, study illustrated modulation miR‐185/ DNMT1/ pathway exerted summary, finding displayed novel regulatory mechanism for fibrosis, which provided new potential therapeutic target

Language: Английский

LncRNA-Meg3 promotes Nlrp3-mediated microglial inflammation by targeting miR-7a-5p DOI
Jiao Meng, Ting Ding, Yuhua Chen

et al.

International Immunopharmacology, Journal Year: 2020, Volume and Issue: 90, P. 107141 - 107141

Published: Nov. 12, 2020

Language: Английский

Citations

55
Deregulated expression of the imprinted DLK1-DIO3 region in glioblastoma stemlike cells: tumor suppressor role of lncRNA MEG3 DOI Creative Commons
Mariachiara Buccarelli, Valentina Lulli, Alessandro Giuliani

et al.

Neuro-Oncology, Journal Year: 2020, Volume and Issue: 22(12), P. 1771 - 1784

Published: May 21, 2020

Glioblastoma (GBM) stemlike cells (GSCs) are thought to be responsible for the maintenance and aggressiveness of GBM, most common primary brain tumor in adults. This study aims at elucidating involvement deregulations within imprinted delta-like homolog 1 gene‒type III iodothyronine deiodinase gene (DLK-DIO3) region on chromosome 14q32 GBM pathogenesis.Real-time PCR analyses were performed GSCs tissues. Methylation analyses, expression, reverse-phase protein array profiles used investigate suppressor function maternally expressed 3 (MEG3).Loss expression genes noncoding RNAs DLK1-DIO3 was observed tissues compared with normal brain. downregulation is mainly mediated by epigenetic silencing. Kaplan-Meier analysis indicated that low MEG3 MEG8 long (lnc)RNAs significantly correlated short survival patients. restoration impairs tumorigenic abilities vitro inhibiting cell growth, migration, colony formation decreases vivo reducing infiltrative growth. These effects associated modulation involved adhesion epithelial-to-mesenchymal transition (EMT).In acts as a regulating adhesion, EMT, proliferation, thus providing potential candidate novel therapies.

Language: Английский

Citations

51
Long noncoding RNA Meg3 sponges miR-708 to inhibit intestinal tumorigenesis via SOCS3-repressed cancer stem cells growth DOI Creative Commons
Shuo Zhang, Weiwei Ji, Wei Wei

et al.

Cell Death and Disease, Journal Year: 2021, Volume and Issue: 13(1)

Published: Dec. 21, 2021

Abstract Background Colorectal cancer (CRC) remains the most common gastrointestinal and a leading cause of deaths worldwide, with showing pathologies indicating malignant transformation early stage intestinal stem cells. The long non-coding RNA Meg3 , which functions as tumor suppressor, has been reported to be abnormal in multiple tumorigenesis events; however, underlying mechanism by contributes proliferation colonic cells unclear. Methods We analyzed expression levels miR-708 SOCS3 samples from Apc loss-of-function ( min ) mice patients CRC, particularly crypt AMO/DSS-induced model (in vivo) organoid culture system vitro) were used explore effect / /SOCS3 axis on colon. In vitro, we performed RNApull-down, immunoprecipitation, luciferase reporter assays using DLD1 RKO cell lines. Findings signaling plays critical role CRC development. Our data showed negatively correlate both clinical mouse model, indicated that acts competitive endogenous (ceRNA) . Then, served an oncogene, inducing neoplasia cultured organoids. Put together, appears promote targeting SOCS3/STAT3 signaling. Interpretation These revealed sponges inhibit development via SOCS3-mediated repression provides potential targets for diagnosis treatment CRC.

Language: Английский

Citations

42
Long non-coding RNAs in cancer: multifaceted roles and potential targets for immunotherapy DOI
Lokesh Kadian, Deepika Verma, Neelam Lohani

et al.

Molecular and Cellular Biochemistry, Journal Year: 2024, Volume and Issue: 479(12), P. 3229 - 3254

Published: Feb. 28, 2024

Language: Английский

Citations

8
lncRNA-MEG3 Suppresses the Proliferation and Invasion of Melanoma by Regulating CYLD Expression Mediated by Sponging miR-499-5p DOI Creative Commons
Jianwen Long,

Xianming Pi

BioMed Research International, Journal Year: 2018, Volume and Issue: 2018, P. 1 - 15

Published: Jan. 1, 2018

The abnormal expression of long noncoding RNA- (lncRNA-) MEG3 was clearly identified in a number malignant tumors, but the specific function remains unknown melanoma until now. research attempts to explore effects on growth and metastasis melanoma. miR-499-5p were determined by qRT-PCR method. Western blotting assay applied detect protein expression. Luciferase reporter used assess correlation between CYLD miR-499-5p. Cell growth, cell cycle, apoptosis examined CCK-8 assay, EdU flow cytometry respectively. invasion ability cells investigated wound-healing Transwell assays. effect vivo chemosensitivity detected xenograft animal model assay. As result, decreased tissues lines. level significantly associated with poor prognosis. could bind mRNA contained binding site reduced elevated western blot confirmed that regulated sponging Functionally, upregulation inhibited proliferation, invasion, migration, enhanced apoptosis, arrested E-cadherin, N-cadherin, cyclin D1 regulating mediated Importantly, overexpression suppressed tumor improved chemotherapy sensitivity A375 cisplatin 5-FU treatment. In conclusion, has crucial tumorigenesis melanoma, may be potential therapeutic target treatment

Language: Английский

Citations

53
The Role of Long Non-Coding RNAs (lncRNAs) in the Development and Progression of Fibrosis Associated with Nonalcoholic Fatty Liver Disease (NAFLD) DOI Creative Commons

Amanda Hanson,

Danielle Wilhelmsen,

Johanna K. DiStefano

et al.

Non-Coding RNA, Journal Year: 2018, Volume and Issue: 4(3), P. 18 - 18

Published: Aug. 21, 2018

Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of conditions ranging from hepatic steatosis to inflammation (nonalcoholic steatohepatitis or NASH) with without fibrosis, in the absence significant alcohol consumption. The presence fibrosis NASH patients is associated greater liver-related morbidity and mortality; however, molecular mechanisms underlying development cirrhosis NAFLD remain poorly understood. Long non-coding RNAs (lncRNAs) are emerging as key contributors biological processes that underpinning initiation progression fibrosis. This review summarizes experimental findings have been obtained date animal models We also discuss potential applicability circulating lncRNAs serve biomarkers for diagnosis prognosis A better understanding role played by critical identification novel therapeutic targets drug improved, noninvasive methods diagnosis.

Language: Английский

Citations

53
LncRNA MEG3 enhances 131I sensitivity in thyroid carcinoma via sponging miR-182 DOI
Y Liu,

Peiru Yue,

Tao Zhou

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2018, Volume and Issue: 105, P. 1232 - 1239

Published: June 22, 2018

Language: Английский

Citations

47
Autophagy-Modulating Long Non-coding RNAs (LncRNAs) and Their Molecular Events in Cancer DOI Creative Commons
Md Zahirul Islam Khan, Shing Yau Tam, Hkw Law

et al.

Frontiers in Genetics, Journal Year: 2019, Volume and Issue: 9

Published: Jan. 14, 2019

Cancer is a global threat of health. incidence and death also increasing continuously because poor understanding diseases. Although, traditional treatments (surgery, radiotherapy chemotherapy) are effective against primary tumours, rate metastasis development where have failed. Autophagy conserved regulatory process eliminating proteins damaged organelles. Numerous research revealed that autophagy has dual sword mechanisms including cancer progressions suppressions. In most the cases, it maintains homeostasis microenvironment by providing nutritional supplement under starvation hypoxic conditions. Over past few decades, stunning evidence disclosed significant roles long non-coding RNAs (lncRNAs) in regulation autophagy. LncRNAs RNA containing more than 200 nucleotides, which no protein-coding ability but they found to be expressed cancers. It proved that, autophagy-modulating lncRNAs impacts on pro-survival or pro-death this review, we highlighted recently identified lncRNAs, their signaling transduction mechanism cancer. This review will explore newly emerging knowledge genetics may provide novel targets for therapy.

Language: Английский

Citations

43
Aberrant methylation-mediated downregulation of lncRNA SSTR5-AS1 promotes progression and metastasis of laryngeal squamous cell carcinoma DOI Creative Commons
Baoshan Wang, Lei Zhao,

Weiwei Chi

et al.

Epigenetics & Chromatin, Journal Year: 2019, Volume and Issue: 12(1)

Published: June 13, 2019

Laryngeal squamous cell carcinoma (LSCC) is among the most common malignant tumors with poor prognosis. Accumulating evidences have identified important roles of long noncoding RNAs (lncRNAs) in initiation and progression various cancer types; however, global lncRNAs expression profile for metastatic LSCC limited. In present study, we screen profiles advanced patients paired tumor tissues corresponding normal by microarrays. We identify numerous differentially expressed transcripts, after necessary verification transcripts expanded samples, experimentally validate patterns remarkable low gene, SSTR5, its antisense lncRNA, SSTR5-AS1. Downregulation SSTR5 detected laryngeal cells. Aberrant DNA hypermethylation CpG sites clustered exon 1 accumulation inactive histone modifications at promoter region may be epigenetic mechanisms inactivation LSCC. SSTR5-AS1 play antitumor role regulated same SSTR5. inhibits cells proliferation, migration, invasion. increases enrichment MLL3 H3K4me3 interacting further induces transcription Furthermore, interacts recruits TET1 to target gene E-cadherin activate expression. These findings suggest that mRNAs potential biomarkers LSCC, act as a suppressor well biomarker therapy.

Language: Английский

Citations

43
Dysregulation of lncRNAs in Rheumatoid Arthritis: Biomarkers, Pathogenesis and Potential Therapeutic Targets DOI Creative Commons
Chenggui Miao, Liangliang Bai, Yaru Yang

et al.

Frontiers in Pharmacology, Journal Year: 2021, Volume and Issue: 12

Published: March 12, 2021

Rheumatoid arthritis (RA) is a chronic autoimmune disease of unknown etiology, mainly manifested by persistent abnormal proliferation fibroblast-like synoviocytes (FLSs), inflammation, synovial hyperplasia and cartilage erosion, accompanied joint swelling destruction. Abnormal expression or function long noncoding RNAs (lncRNAs) are closely related to human diseases, including cancers, mental diseases others. The sequence spatial structure lncRNAs, the disorder interaction with binding protein will lead change gene in way epigenetic modification. Increasing evidence demonstrated that lncRNAs were involved activation FLSs, which played key role pathogenesis RA. In this review, research progress RA was systematically summarized, diagnosis RA, regulatory mechanism intervention treatment Furthermore, activated signal pathways, DNA methylation other have also been overview review.

Language: Английский

Citations

39