scholarly journals Long non-coding RNA PVT1, a molecular sponge of miR-26b, is involved in the progression of hyperglycemia-induced collagen degradation in human chondrocytes by targeting CTGF/TGF-β signal ways

2019 ◽  
Vol 26 (3) ◽  
pp. 204-214 ◽  
Author(s):  
Luo-Bin Ding ◽  
Yao Li ◽  
Guang-Yuan Liu ◽  
Tai-Hang Li ◽  
Feng Li ◽  
...  
Keyword(s):  
Type Ii Collagen ◽  
Collagen Degradation ◽  
Human Chondrocytes ◽  
Luciferase Reporter ◽  
Type Ii ◽  
Over Expression ◽  
Knee Oa ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Tgf Β1

The current study was conducted to investigate the role of long non-coding RNA PVT1 in hyperglycemia-triggered human osteoarthritis (OA) chondrocytes. Cartilage from knee OA patients with and without diabetes, as well as normal cartilage, was obtained. Isolated human chondrocytes were treated with 30 nM of Glc with or without pioglitazone. The expression levels of PVT1, miR-26b, and type II collagen were determined by RT-PCR. Type II collagen was detected by immunocytochemistry and chondrocytes were stained with Alcian blue. Moreover, the interaction among PVT1, miR-26b, and CTGF was examined using bioinformatics, FISH, RIP, RNA-pull down, and luciferase reporter assays. Over-expression of PVT1 and miR-26b were performed and expressions of CTGF, TGF-β1, SMAD3, MMP-13, and type II collagen proteins were examined. Significantly higher expression of PVT1 was observed in diabetic OA. High Glc induced the elevated expression of PVT1, CTGF, TGF-β1, IL-6, and MMP-13, as well as decreased expression of type II collagen and miR-26b. These alterations could be reversed by pioglitazone. PVT1 acted as a sponge for miR-26b to facilitate CTGF expression. Over-expression of PVT1 increased the expressions of CTGF, TGF-β1, SMAD3, and MMP-13 and decreased expression of type II collagen. Our findings confirmed that PVT1 is involved in the hyperglycemia-induced collagen degradation, via the miR-26b-CTGF-TGF-β1-axis.

scholarly journals Long Noncoding RNA SNHG10 Inhibits Renal Fibrosis By Negatively Regulating MiR-378b Expression

2021 ◽  
Author(s):  
Jian Hao ◽  
Yun Zhou ◽  
Weimin Yu ◽  
Hui Li ◽  
Dandan He
Keyword(s):  
Renal Fibrosis ◽  
Noncoding Rna ◽  
Luciferase Reporter ◽  
Tissue Samples ◽  
Non Coding Rna ◽  
Promising Therapeutic Target ◽  
Fibronectin Expression ◽  
Long Non Coding Rna ◽  
Tgf Β1 ◽  
Dual Luciferase Reporter Assay

Abstract Background: LncRNA have been increasingly shown that plays pivotal roles in the development of various diseases, including renal fibrosis. Nevertheless, the pathological function of Long non-coding RNA SNHG10 (SNHG10) in the renal fibrosis remains obscure.Methods: We detected the expression levels of SNHG10 in the tissue samples and cell lines via RT-qPCR analysis. The functions of SNHG10 on the progression of renal fibrosis were examined by CCK-8, EdU, dual luciferase reporter and immunofluorescence analyses.Results: In the present study, SNHG10, production of extracellular matrix (ECM), including α-SMA and Fibronectin levels were significantly increased in HK-2 cells after TGF-β stimulation. Ectopic of SNHG10 inhibited cell proliferation and inhibits theα-SMA and Fibronectin expression of TGF-β1-induced HK-2 cells. In addition, bioinformatics analysis and dual luciferase reporter assay indicated that miR-378b was a target gene of SNHG10. Mechanistically, miR-378b overexpression abolished the repressive effects of SNHG10 on TGF-β1-induced HK-2 cells.Conclusion: SNHG10 plays an anti-fibrotic effect through suppression of miR-378b expression in renal fibrosis, which provides a promising therapeutic target for the treatment of renal fibrosis.

scholarly journals LncRNA ACTA2-AS1 suppress colon adenocarcinoma progression by sponging miR-4428 upregulation BCL2L11

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qingyun Pan ◽  
Ying Huang ◽  
Yirui Wang ◽  
Deke Li ◽  
Changjiang Lei
Keyword(s):  
Cell Proliferation ◽  
Colony Formation ◽  
Colon Adenocarcinoma ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Over Expression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background Long non-coding RNA is considered to be essential to modulate the development and progression of human malignant cancers. And long non-coding RNA can act as crucial modulators by sponging the corresponding microRNA in tumorigenesis. We aimed to elucidate the function of ACTA2-AS1 and its molecular mechanism in colon adenocarcinoma. Materials and methods The expression of ACTA2-AS1, miR-4428 and BCL2L11 in colon adenocarcinoma tissues were detected via qRT-PCR. SW480 and HT29 cells were transfected with shRNA ACTA2-AS1, OE ACTA2-AS1, miRNA mimics of miR-4428, miR-4428 inhibitor, si-BCL2L11 and over-expression of si-BCL2L11. Cell proliferation, colony formation and apoptosis were respectively assessed using CCK-8 assay, colony assay and flow cytometry. Luciferase reporter assay was performed to verify the targets of ACTA2-AS1 and miR-4428. Tumor subcutaneous xenograft mode was constructed to explore tumor growth in vivo. Results ACTA2-AS1 was obviously downregulated in human colon adenocarcinoma tissues and colon adenocarcinoma cell lines. Silence or over-expression of ACTA2-AS1 promoted or inhibited cell proliferation and colony formation abilities, and regulated apoptosis. The silence of ACTA2-AS1 resulted in the decrease of Bax and increase of Bal2, while restored in OE ACTA2-AS1 group when compared with the control transfected cells. In addition, luciferase reporter assay revealed that ACTA2-AS1 interacted with miR-4428 and suppressed its expression. miR-4428 could bind to 3ʹ untranslated region of BCL2L11 and modulated the expression of BCL2L11 negatively. Knockdown of ACTA2-AS1 and over-expression of BCL2L11 reversed the biological function that ACTA2-AS1 mediated by knockdown ACTA2-AS1 alone. Conclusion Our data demonstrated that ACTA2-AS1 could suppress colon adenocarcinoma progression via sponging miR-4428 to regulate BCL2L11 expression.

scholarly journals LncRNA TUG1 Regulates Proliferation of Cardiac Fibroblast via the miR-29b-3p/TGF-β1 Axis

2021 ◽  
Vol 8 ◽  
Author(s):  
Yini Guo ◽  
Zongli Sun ◽  
Minghe Chen ◽  
Junjie Lun
Keyword(s):  
Target Gene ◽  
Cardiac Fibroblasts ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Healthy Controls ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Taurine Upregulated Gene 1 ◽  
Tgf Β1

Background: Atrial fibrillation (AF) is a very common clinical arrhythmia, accompanied by the overproliferation of cardiac fibroblasts (CFs). This study aimed to investigate the role of the long non-coding RNA(lncRNA) taurine upregulated gene 1 (TUG1) in the proliferation of CFs and further investigated its underlying mechanism.Methods: One hundred four paroxysmal AF patients and 94 healthy controls were recruited. Human cardiac fibroblasts (HCFs) were applied to establish an AF cell model through treatment with angiotensin II (AngII). qRT-PCR was used for the measurement of gene levels. The cell proliferation was detected by cell counting kit-8 (CCK-8). Luciferase reporter assay was performed for target gene analysis.Results: Elevated levels of TUG1 and low expression of miR-29b-3p were detected in the serum of AF patients compared with the healthy controls. Pearson's correlation analysis exhibited an inverse relationship between TUG1 and miR-29b-3p expression in AF patients (r = −7.106, p < 0.001). Knockdown of TUG1 inhibited AngII-induced CF proliferation. Taurine upregulated gene 1 (TUG1) functions as a competing endogenous RNA (ceRNA) for miR-29b-3p, and downregulation of miR-29b-3p reversed the role of TUG1 in CF proliferation. TGF-β1 is a direct target gene of miR-29b-3p.Conclusions: Long non-coding RNA taurine upregulated gene 1 is a key regulator in the occurrence of AF. Slicing TUG1 inhibits CF proliferation by regulating the miR-29b-3p/TGF-β1 axis.

Long Non-Coding RNA Small Nucleolar RNA Host Gene 14 Enhances Pancreatic-β-Cell Function by Sponging MicroRNA-206 and Thereby Upregulating Insulin-Like Growth Factor-1

2021 ◽  
Vol 11 (11) ◽  
pp. 2286-2293
Author(s):  
Zheng Mao ◽  
Zhen Li ◽  
Zengkun Qian ◽  
Jingjing Zhou ◽  
Xiaoqin Li ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Growth Factor ◽  
Peripheral Blood ◽  
Luciferase Reporter ◽  
Diabetic Patients ◽  
Potential Candidate ◽  
Insulin Like Growth Factor ◽  
Over Expression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Diabetes mellitus (DM) characterised by pancreatic β-cell dysfunction and insulin resistance is already prevalent worldwide, and the complications of DM increased the mortality of diabetic patients. More and more reports showed that long non-coding RNA (lncRNA) plays key roles in DM, and in this study we explored the effect of long non-coding RNA SNHG14 (SNHG14) in DM. Quantitative reverse transcription PCR (qRT-PCR) was used to analyze the expression of SNHG14 and microRNA (miR)-206 in peripheral blood from 60 pairs of healthy and DM samples. Then the effect of SNHG14 on the insulin secretion of pancreatic β-cells was investigated. Moreover, the effects of SNHG14 on the viability and apoptosis of pancreatic β-cells were determined by 3-(4, 5)-dimethylthiahiazo (-z-y1)-3, 5-di- phenytetrazoliumromide (MTT) assay and flow cytometry (FCM) respectively using INS-1 cells transfected with SNHG14-plasmid and/or miR-206 mimic. Bioinformatics and Daul luciferase reporter assay were used to confirm the direct target of miR-206. Our data showed that SNHG14 level was decreased but miR-206 was increased significantly in the peripheral blood of DM patients. Furthermore, over-expression of SNHG14 enhanced insulin secretion and cell viability but inhibited apoptosis of pancreatic β-cells, whereas, miR-206 over-expression reversed these effects. In addition, insulin-like growth factor-1 (IGF1) was proved to be regulated by miR-206 negatively and over-expression of SNHG14 increased the expression of IGF1 and IGF1R in pancreatic β-cells. In conclusion, we found that SNHG14 was significantly down-regulated in DM patients, and SNHG14/miR-206/IGF1 may serve as a potential candidate for the clinical target of DM.

scholarly journals Long non-coding RNA LINC00346 contributes to cisplatin resistance in nasopharyngeal carcinoma by repressing miR-342-5p

Open Biology ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 190286 ◽  
Author(s):  
Zheqing Cui ◽  
Tian Pu ◽  
Yujie Zhang ◽  
Jia Wang ◽  
Yulin Zhao
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Cisplatin Resistance ◽  
Chemotherapy Resistance ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Over Expression ◽  
Non Coding Rna ◽  
Rna Immunoprecipitation ◽  
Cisplatin Sensitivity ◽  
Long Non Coding Rna

Cisplatin has been used as the first-line chemotherapy to treat advanced nasopharyngeal carcinoma (NPC), while acquired cisplatin resistance resulting from epigenetic regulation is not well understood. The relative expression of LINC00346 was detected in healthy persons, cisplatin-sensitive (CS) patients and cisplatin-resistant (CR) patients. The regulatory effect of LINC00346 on the proliferation was detected by cell-counting kit-8. Apoptosis was assayed by histone/DNA ELISA and Caspase-3 activity. Clonal formation and cisplatin resistance were also deciphered. Luciferase reporter and RNA immunoprecipitation assay were adopted to study the interaction between LINC00346 and miR-342-5p. LINC00346 was highly expressed in NPC patients, especially in CR patients, which was associated with cisplatin resistance and poor prognosis. Inhibition of LINC00346 expression promoted cisplatin sensitivity of NPC cells, while LINC00346 over-expression promoted cisplatin resistance of NPC cells. miR-342-5p expression was negatively correlated with cisplatin resistance, and microRNA-342-5p siRNAs treatment could rescue the cisplatin resistance diminished by LINC00346 inhibition. It was further found that miR-342-5p was negatively regulated by LINC00346. In conclusion, LINC00346 regulates the cisplatin resistance of NPC cells by inhibiting miR-342-5p, which could provide a potential target for chemotherapy resistance.

scholarly journals LncRNA PVT1 promotes cervical cancer progression by sponging miR-503 to upregulate ARL2 expression

2021 ◽  
Vol 16 (1) ◽  
pp. 1-13
Author(s):  
Weiwei Liu ◽  
Dongmei Yao ◽  
Bo Huang
Keyword(s):  
Cervical Cancer ◽  
Cancer Progression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Nude Mouse Model ◽  
Western Blot Assay ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Cervical cancer (CC) is a huge threat to the health of women worldwide. Long non-coding RNA plasmacytoma variant translocation 1 gene (PVT1) was proved to be associated with the development of diverse human cancers, including CC. Nevertheless, the exact mechanism of PVT1 in CC progression remains unclear. Levels of PVT1, microRNA-503 (miR-503), and ADP ribosylation factor-like protein 2 (ARL2) were measured by quantitative reverse transcription-polymerase chain reaction or western blot assay. 3-(4,5)-Dimethylthiazole-2-y1)-2,5-biphenyl tetrazolium bromide (MTT) and flow cytometry were used to examine cell viability and apoptosis, respectively. For migration and invasion detection, transwell assay was performed. The interaction between miR-503 and PVT1 or ARL2 was shown by dual luciferase reporter assay. A nude mouse model was constructed to clarify the role of PVT1 in vivo. PVT1 and ARL2 expressions were increased, whereas miR-503 expression was decreased in CC tissues and cells. PVT1 was a sponge of miR-503, and miR-503 targeted ARL2. PVT1 knockdown suppressed proliferation, migration, and invasion of CC cells, which could be largely reverted by miR-503 inhibitor. In addition, upregulated ARL2 could attenuate si-PVT1-mediated anti-proliferation and anti-metastasis effects on CC cells. Silenced PVT1 also inhibited CC tumor growth in vivo. PVT1 knockdown exerted tumor suppressor role in CC progression via the miR-503/ARL2 axis, at least in part.

scholarly journals Senescence associated long non-coding RNA 1 regulates cigarette smoke-induced senescence of type II alveolar epithelial cells through sirtuin-1 signaling

2021 ◽  
Vol 49 (2) ◽  
pp. 030006052098604
Author(s):  
Dong Yuan ◽  
Yuanshun Liu ◽  
Mengyu Li ◽  
Hongbin Zhou ◽  
Liming Cao ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Sirtuin 1 ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Objective The primary aim of our study was to explore the mechanisms through which long non-coding RNA (lncRNA)-mediated sirtuin-1 (SIRT1) signaling regulates type II alveolar epithelial cell (AECII) senescence induced by a cigarette smoke-media suspension (CSM). Methods Pharmacological SIRT1 activation was induced using SRT2104 and senescence-associated lncRNA 1 (SAL-RNA1) was overexpressed. The expression of SIRT1, FOXO3a, p53, p21, MMP-9, and TIMP-1 in different groups was detected by qRT-PCR and Western blotting; the activity of SA-β gal was detected by staining; the binding of SIRT1 to FOXO3a and p53 gene transcription promoters was detected by Chip. Results We found that CSM increased AECII senescence, while SAL-RNA1 overexpression and SIRT1 activation significantly decreased levels of AECII senescence induced by CSM. Using chromatin immunoprecipitation, we found that SIRT1 bound differentially to transcriptional complexes on the FOXO3a and p53 promoters. Conclusion Our results suggested that lncRNA-SAL1-mediated SIRT1 signaling reduces senescence of AECIIs induced by CSM. These findings suggest a new therapeutic target to limit the irreversible apoptosis of lung epithelial cells in COPD patients.

Long Non-Coding RNA ARAP1-AS1 Facilitates the Progression of Cervical Cancer by Regulating miR-149-3p and POU2F2

Pathobiology ◽  
2021 ◽  
pp. 1-12
Author(s):  
Ling Zhou ◽  
Xiao-li Xu
Keyword(s):  
Cervical Cancer ◽  
Tumor Model ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Injection Model ◽  
Rna Immunoprecipitation ◽  
Long Non Coding Rna

<b><i>Background:</i></b> Emerging research has demonstrated that long non-coding RNAs (lncRNAs) attach great importance to the progression of cervical cancer (CC). LncRNA ARAP1-AS1 was involved in the development of several cancers; however, its role in CC is far from being elucidated. <b><i>Methods:</i></b> Real-time PCR (RT-PCR) was employed to detect ARAP1-AS1 and miR-149-3p expression in CC samples. CC cell lines (HeLa and C33A cells) were regarded as the cell models. The biological effect of ARAP1-AS1 on cancer cells was measured using CCK-8 assay, colony formation assay, flow cytometry, Transwell assay and wound healing assay in vitro, and subcutaneous xenotransplanted tumor model and tail vein injection model in vivo. Furthermore, interactions between ARAP1-AS1 and miR-149-3p, miR-149-3p and POU class 2 homeobox 2 (POU2F2) were determined by bioinformatics analysis, qRT-PCR, Western blot, luciferase reporter and RNA immunoprecipitation assay, respectively. <b><i>Results:</i></b> The expression of ARAP1-AS1 was enhanced in CC samples, while miR-149-3p was markedly suppressed. Additionally, ARAP1-AS1 overexpression enhanced the viability, migration, and invasion of CC cells. ARAP1-AS1 downregulated miR-149-3p via sponging it. ARAP1-AS1 and miR-149-3p exhibited a negative correlation in CC samples. On the other hand, ARAP1-AS1 enhanced the expression of POU2F2, which was validated as a target gene of miR-149-3p. <b><i>Conclusion:</i></b> ARAP1-AS1 was abnormally upregulated in CC tissues and indirectly modulated the POU2F2 expression via reducing miR-149-3p expression. Our study identified a novel axis, ARAP1-AS1/miR-149-3p/POU2F2, in CC tumorigenesis.

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