scholarly journals LncRNA BISPR promotes the progression of thyroid papillary carcinoma by regulating miR-21-5p

2018 ◽  
Vol 32 ◽  
pp. 205873841877265 ◽  
Author(s):  
Hong Zhang ◽  
Yuechang Cai ◽  
Li Zheng ◽  
Zhanlei Zhang ◽  
Xiaofeng Lin ◽  
...  
Keyword(s):  
Cell Viability ◽  
Papillary Carcinoma ◽  
Quantitative Polymerase Chain Reaction ◽  
B Cell Lymphoma ◽  
Thyroid Papillary Carcinoma ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Aberrant Expression ◽  
Mouse Xenograft Model ◽  
Thyroid Papillary

Our study attempted to verify the effect of lncRNA BST2 interferon-stimulated positive regulator (BISPR) on cell viability, propagation and invasiveness of thyroid papillary carcinoma (TPC) and the interactive relationship between BISPR and miR-21-5p. Microarray analyzed the aberrant expression lncRNA BISPR in TPC. BISPR and miR-21-5p as well as B-cell lymphoma-2 (Bcl-2) expressions in TPC cells were determined by quantitative polymerase chain reaction (qRT-PCR) and Western blot. Cell counting kit-8 (CCK-8) assay, dual luciferase reporter assay, and transwell assay were conducted to manifest cell viability, propagation, and invasiveness of TPC cells. Flow cytometry was performed to determine the apoptosis and cell cycle of TPC cells. Mouse xenograft model was built to testify the effect of BISPR on tumor growth. BISPR in TPC tissues was over-expressed. BISPR knockdown restrained the propagation and invasiveness and enhanced the iodine uptake of TPC cells. The tumor-forming rate reduced after BISPR knockdown. In addition, miR-21-5p was lowly expressed in cancer tissues. BISPR promoted the development of TPC cells by inhibiting miR-21-5p expression. Bcl-2 was suppressed by miR-21-5p and sh-BISPR. BISPR, which was over-expressed in TPC, improved TPC cell viability, propagation, and invasiveness. MiR-21-5p was lowly expressed in TPC which inhibited Bcl-2 expression. BISPR stimulated propagation and invasiveness of TPC cells by depressing miR-21-5p.

scholarly journals m(6)A Modification of lncRNA NEAT1 Regulates Chronic Myelocytic Leukemia Progression via miR-766-5p/CDKN1A Axis

2021 ◽  
Vol 11 ◽  
Author(s):  
Fang-Yi Yao ◽  
Cui Zhao ◽  
Fang-Min Zhong ◽  
Ting-Yu Qin ◽  
Fang Wen ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Lines ◽  
Mononuclear Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Critical Role ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Aberrant Expression ◽  
Hematopoietic Stem ◽  
Expression Levels

BackgroundChronic myeloid leukemia (CML) is an acquired hematopoietic stem malignant disease originating from the myeloid system. Long non-coding RNAs (lncRNAs) have been widely explored in cancer tumorigenesis. However, their roles in CML remain largely unclear.MethodsThe peripheral blood mononuclear cells (PBMCs) and CML cell lines (K562, KCL22, MEG01, BV173) were collected for in vitro research. Real-time quantitative polymerase chain reaction was used to determine the mRNA expression levels. Cell viability and apoptosis were analyzed by cell counting kit 8 and flow cytometry assays. The targeting relationships were predicted using Starbase and TargetScan and ulteriorly verified by RNA pull-down and luciferase reporter assays. Western blotting assay was performed to assess the protein expressions. N6-methyladenosine (m6A) modification sites were predicted by SRAMP and confirmed by Methylated RNA immunoprecipitation (MeRIP) assay.ResultsLncRNA nuclear-enriched abundant transcript 1 (NEAT1) expression levels were decreased in the CML cell lines and PBMCs of CML patients. Moreover, METTL3-mediated m6A modification induced the aberrant expression of NEAT1 in CML. Overexpression of NEAT1 inhibited cell viability and promoted the apoptosis of CML cells. Additionally, miR-766-5p was upregulated in CML PBMCs and abrogated the effects of NEAT1 on cell viability and apoptosis of the CML cells. Further, CDKN1A was proved to be the target gene of miR-766-5p and was downregulated in the CML PBMCs. Knockdown of CDKN1A reversed the effects of NEAT1.ConclusionThe current research elucidates a novel METTL3/NEAT1/miR-766-5p/CDKN1A axis which plays a critical role in the progression of CML.

LINC00265 promotes the viability, proliferation, and migration of bladder cancer cells via the miR-4677-3p/FGF6 axis

2021 ◽  
pp. 096032712110434
Author(s):  
Yunlai Zhi ◽  
Fanghu Sun ◽  
Chengkuan Cai ◽  
Haitao Li ◽  
Kunpeng Wang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Viability ◽  
Messenger Rna ◽  
Binding Capacity ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Xenograft Tumor ◽  
And Migration ◽  
Proliferation And Migration

Background Bladder cancer (BCa) is a common genitourinary malignancy with higher incidence in males. Long intergenic non-protein coding RNA 265 (LINC00265) is identified as an oncogene in many malignancies, while its role in BCa development remains unknown. Purpose To explore the functions and mechanism of LINC00265 in BCa Research Design Reverse transcription quantitative polymerase chain reaction was performed to examine LINC00265 expression in BCa cells. Cell counting kit-8 assays, colony formation assays, TdT-mediated dUTP Nick-End Labeling assays, and Transwell assays were conducted to examine BCa cell viability, proliferation, apoptosis, and migration. Luciferase reporter assays and RNA immunoprecipitation assays were carried out to explore the binding capacity between miR-4677-3p and messenger RNA fibroblast growth factor 6 (FGF6) (or LINC00265). Xenograft tumor model was established to explore the role of LINC00265 in vivo. Results LINC00265 was highly expressed in BCa cells. LINC00265 knockdown inhibited xenograft tumor growth and BCa cell viability, proliferation and migration while enhancing cell apoptosis. Moreover, LINC00265 interacted with miR-4677-3p to upregulate the expression of FGF6. FGF6 overexpression reversed the suppressive effect of LINC00265 knockdown on malignant phenotypes of BCa cells. Conclusions LINC00265 promotes the viability, proliferation, and migration of BCa cells by binding with miR-4677-3p to upregulate FGF6 expression.

scholarly journals Exhausting circ_0136474 and Restoring miR-766-3p Attenuate Chondrocyte Oxidative Injury in IL-1β-Induced Osteoarthritis Progression Through Regulating DNMT3A

2021 ◽  
Vol 12 ◽  
Author(s):  
Haiquan Zhu ◽  
Shaobo Zhu ◽  
Xiuchao Shang ◽  
Xiangsheng Meng ◽  
Sheng Jing ◽  
...  
Keyword(s):  
Cell Viability ◽  
Dna Methyltransferase ◽  
Direct Interaction ◽  
B Cell Lymphoma ◽  
Oxidative Injury ◽  
Cell Counting ◽  
Nuclear Antigen ◽  
Luciferase Reporter ◽  
Matrix Metalloproteinase 1 ◽  
Collagen Ii

Circular RNA circ_0136474 is a new contributor of human osteoarthritis (OA) by suppressing chondrocyte proliferation. However, its role and mechanism in OA chondrocyte injury remain ill defined. Herein, we performed real-time quantitative PCR to detect RNA expression of circ_0136474, microRNA (miR)-766-3p, and DNA methyltransferase 3A (DNMT3A) and utilized Western blotting to measure protein expression of DNMT3A, matrix metalloproteinase-1 (MMP1), MMP13, collagen II, proliferating cell nuclear antigen (PCNA) and B cell lymphoma (Bcl)-2, and Bcl-2-associated X protein (Bax). Direct interaction between miR-766-3p and circ_0136474 or DNMT3A was confirmed by bioinformatics algorithms, dual-luciferase reporter assay, and RNA immunoprecipitation. Functional experiments including cell counting kit-8 assay, flow cytometry, and special assay kits were employed to measure oxidative injury in interleukin (IL)-1β-induced OA-like chondrocytes. First, IL-1β administration induced cell viability inhibition, collagen II suppression, and promotion of MMP1 and MMP13 in human chondrocyte CHON-001 cells. Expression of circ_0136474 and DNMT3A was upregulated, and miR-766-3p was downregulated in human OA cartilages and IL-1β-induced CHON-001 cells. Functionally, both blocking circ_0136474 and upregulating miR-766-3p could rescue cell viability and levels of PCNA, Bcl-2, reduced glutathione (GSH), and total superoxide dismutase (SOD), and attenuate apoptosis rate and levels of Bax, reactive oxygen species (ROS), and lipid peroxidation malondialdehyde (MDA). Mechanically, circ_0136474 served as miR-766-3p sponge to govern miR-766-3p-targeted DNMT3A expression. Accidently, restoring DNMT3A counteracted the miR-766-3p upregulation role, and silencing miR-766-3p weakened circ_0136474 knockdown effect in IL-1β-induced CHON-001 cells. In conclusion, exhausting circ_0136474 could mitigate OA chondrocyte oxidative injury through regulating miR-766-3p/DNMT3A axis.

Liver microRNA-29b-3p positively correlates with relative enhancement values of magnetic resonance imaging and represses liver fibrosis

2020 ◽  
Vol 168 (6) ◽  
pp. 603-609
Author(s):  
Xijun Gong ◽  
Xiaolin Wang ◽  
Fangfang Zhou
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Liver Fibrosis ◽  
Cell Viability ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Resonance Imaging ◽  
Relative Enhancement ◽  
Tgf Β1

Abstract This study aims to identify potential microRNAs (miRNAs) contribute to liver fibrosis progression and investigate how the miRNA is involved. We recruited totally 58 patients. Magnetic resonance imaging was employed to detect fibrosis. Classification of liver fibrosis was carried out by Ishak scoring system. Cell viability was tested using cell counting kit-8. Measurements of mRNA and protein expressions were conducted using real-time quantitative polymerase chain reaction and western blotting. Luciferase reporter assay was recruited for determination of miR-29b-3p targets. We found that relative enhancement (RE) values were reduced with the increases in fibrosis stages and was negatively associated with Ishak scores. In comparison with patients without liver fibrosis, miR-29b-3p level was remarkably reduced in those with liver fibrosis. Its level was found to be positively associated with RE values. Transforming growth factor beta 1 (TGF-β1)-induced hepatic stellate cell (HSC) activation significantly decreased miR-29b-3p expression. However, miR-29b-3p overexpression repressed TGF-β1-induced collagen I protein and alpha-smooth muscle actin (α-SMA) expression. As expected, its overexpression also reduced cell viability. We found that miR-29b-3p directly bind to signal transducer and activator of transcription 3 (STAT3) and suppressed its expression. Our study demonstrates that low expression of miR-29b-3p may contribute to the progression of liver fibrosis by suppressing STAT3.

scholarly journals Hypermethylation of the HIC1 promoter and aberrant expression of HIC1/SIRT1 contribute to the development of thyroid papillary carcinoma

Oncotarget ◽  
2016 ◽  
Vol 7 (51) ◽  
pp. 84416-84427 ◽  
Author(s):  
Wenyi Wu ◽  
Liting Zhang ◽  
Jianqing Lin ◽  
Hanwei Huang ◽  
Bai Shi ◽  
...  
Keyword(s):  
Papillary Carcinoma ◽  
Thyroid Papillary Carcinoma ◽  
Aberrant Expression ◽  
Thyroid Papillary

scholarly journals Long Non-coding RNA MIAT Knockdown Prevents the Formation of Intracranial Aneurysm by Downregulating ENC1 via MYC

2021 ◽  
Vol 11 ◽  
Author(s):  
Xinguo Li ◽  
Hang Zhao ◽  
Jihui Liu ◽  
Jing Tong
Keyword(s):  
Myocardial Infarction ◽  
Endothelial Cells ◽  
Intracranial Aneurysm ◽  
Cell Viability ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Immunoprecipitation Assay

Intracranial aneurysm (IA) is vascular enlargement occurred on the wall of cerebral vessels and can result in fatal subarachnoid hemorrhage when ruptured. Recent studies have supported the important role of long non-coding RNAs (lncRNAs) in IA treatment. This study identified functional significance of lncRNA myocardial infarction associated transcript (MIAT) in IA. Myocardial infarction associated transcript and ectodermal-neural cortex 1 (ENC1) expression was detected by reverse transcription quantitative polymerase chain reaction. Cell counting kit 8 assay flow cytometry were conducted to detect cell viability and apoptosis of endothelial cells in IA. The interaction among MIAT, ENC1, and myelocytomatosis oncogene (MYC) was analyzed by RNA pull down, RNA immunoprecipitation assay, chromatin immunoprecipitation assay, and dual luciferase reporter assay. Intracranial aneurysm was induced by ligating the left carotid artery and the bilateral posterior branch of the renal artery in rats for studying the role of MIAT and ENC1 in vivo. Myocardial infarction associated transcript and ENC1 were upregulated in IA. Endothelial cells in IA presented a decreased cell viability and an increased apoptotic rate. Myocardial infarction associated transcript could regulate the expression of ENC1, and MYC could bind to the promoter region of ENC1. High expression of MIAT increased endothelial cell apoptosis and vascular endothelial injury, while MIAT knockdown was identified to reduce the risk of IA both in vitro and in vivo through regulating ENC1. To sum up, MIAT silencing is preventive for IA occurrence by decreasing the MYC-mediated ENC1 expression, which represents a novel therapeutic target for IA.

Expression of Cytokeratin 19 in the Diagnosis of Thyroid Papillary Carcinoma by Quantitative Polymerase Chain Reaction

2008 ◽  
Vol 14 (2) ◽  
pp. 168-174 ◽  
Author(s):  
John Flanagan ◽  
Pedro Pineda ◽  
Philip Knapp ◽  
Antonio De Las Morenas ◽  
Stephanie Lee ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Papillary Carcinoma ◽  
Quantitative Polymerase Chain Reaction ◽  
Thyroid Papillary Carcinoma ◽  
Cytokeratin 19 ◽  
Chain Reaction ◽  
Thyroid Papillary ◽  
Polymerase Chain

scholarly journals Circ-RNF111 aggravates the malignancy of gastric cancer through miR-876-3p-dependent regulation of KLF12

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Guoxian Wu ◽  
Aimin Zhang ◽  
Yinglin Yang ◽  
Dongping Wu
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Viability ◽  
Colony Formation ◽  
Xenograft Model ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Aberrant Expression

Abstract Background The aberrant expression of circular RNAs (circRNAs) plays vital roles in the advancement of human cancers, including gastric cancer (GC). In this study, the functions of circRNA ring finger protein 111 (circ-RNF111) in GC were investigated. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) assay was performed for the levels of circ-RNF111, microRNA-876-3p (miR-876-3p) and krueppel-like factor 12 (KLF12) mRNA. RNase R assay was conducted for the feature of circ-RNF111. Cell Counting Kit-8 (CCK-8) assay, colony formation assay, wound-healing assay, and transwell assay were applied for cell viability, colony formation, migration, and invasion, respectively. Flow cytometry analysis was used to analyze cell apoptosis and cell cycle process. The glycolysis level was examined using specific commercial kits. Western blot assay was carried out to measure the protein levels of hexokinase 2 (HK-2) and KLF12. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were employed to verify the combination between miR-876-3p and circ-RNF111 or KLF12. Murine xenograft model was constructed for the role of circ-RNF111 in vivo. Immunohistochemistry (IHC) was used for KLF12 level. Results Circ-RNF111 was higher expressed in GC tissues and cells than normal tissues and cells. Silencing of circ-RNF111 restrained cell viability, colony formation, migration, invasion, cell cycle process and glycolysis and induced apoptosis in GC cells in vitro. Circ-RNF111 positively regulated KLF12 expression via absorbing miR-876-3p. MiR-876-3p downregulation reversed the impacts of circ-RNF111 silencing on GC cell malignant phenotypes. MiR-876-3p overexpression repressed GC cell growth, metastasis and glycolysis, inhibited apoptosis and arrested cell cycle, while KLF12 elevation weakened the effects. Besides, circ-RNF111 knockdown inhibited tumor growth in vivo. Conclusion Circ-RNF111 knockdown relieved the development of GC by regulating miR-876-3p/KLF12 axis.

scholarly journals Circular RNA circPVT1 Contributes to Doxorubicin (DXR) Resistance of Osteosarcoma Cells by Regulating TRIAP1 via miR-137

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Dan Li ◽  
Yan Huang ◽  
Gang Wang
Keyword(s):  
Quantitative Polymerase Chain Reaction ◽  
Tumor Model ◽  
B Cell Lymphoma ◽  
Circular Rna ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Osteosarcoma Cells ◽  
Western Blot Assay

Background. Chemoresistance is a major obstacle to the treatment of osteosarcoma patients. Circular RNA (circRNA) circPVT1 has been reported to be related to the doxorubicin (DXR) resistance in osteosarcoma. This study is designed to explore the role and mechanism of circPVT1 in the DXR resistance of osteosarcoma. Methods. circPVT1, microRNA-137 (miR-137), and TP53-regulated inhibitor of apoptosis 1 (TRIAP1) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The protein levels of ATP-binding cassette, subfamily C, member 1 (ABCC1), multidrug resistance-associated protein 1 (MRP-1), cleaved- (c-) caspase-3, B-cell lymphoma-2 (Bcl-2), and TRIAP1 were examined by a western blot assay. Cell viability, proliferation, and apoptosis were detected by cell counting kit-8 (CCK-8), colony formation, and flow cytometry assays, severally. The binding relationship between miR-137 and circPVT1 or TRIAP1 was predicted by starbase 3.0 and then verified by dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. The biological role of circPVT1 in osteosarcoma tumor growth and drug resistance was examined by the xenograft tumor model in vivo. Results. circPVT1 and TRIAP1 were highly expressed, and miR-137 was decreased in DXR-resistant osteosarcoma tissues and cells. Moreover, circPVT1 knockdown could boost DXR sensitivity by inhibiting DXR-caused proliferation and DXR-induced apoptosis in DXR-resistant osteosarcoma cells in vitro. The mechanical analysis discovered that circPVT1 acted as a sponge of miR-137 to regulate TRIAP1 expression. circPVT1 silencing increased the drug sensitivity of osteosarcoma in vivo. Conclusion. circPVT1 boosted DXR resistance of osteosarcoma cells partly by regulating the miR-137/TRIAP1 axis, hinting a promising therapeutic target for the osteosarcoma treatment.

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