cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.17162471
title: Diagnostic significance of microRNA-1255b-5p in prostate cancer patients and its effect on cancer cell function

description: Discerning between indolent and aggressive types is a big challenge of prostate cancer clinically to guide the adequate therapeutic regimen. We aimed to examine the relationship between miR-1255b-p expression and prostate cancer and elucidate the function of miR-1255b-5p in prostate cancer. miR-1255b-5p were measured using Quantitative Real-Time PCR from the blood 103 benign prostate hyperplasia (BPH) and 153 prostate cancer patients (117 indolent cases and 36 upgrading cases). Using receiver operating characteristic (ROC) curve analysis, the discriminating ability of miR-1255b-5p was accessed between BPH and prostate cancer participants, or indolent and aggressive type. Using CCK-8 and Transwell assays, the function of miR-1255b-5p on prostate cancer cells was investigated. The levels of miR-1255b-5p were significantly raised in prostate cancer patients when compared with BPH participants. MiR-1255b-5p level can distinguish prostate cancer patients from BPH or indolent type from aggressive type. Downregulation of miR-1255b-5p can suppress the proliferative, invasive, and migratory capacity, but this effect can be eradicated by <i>EPB41L1</i> inhibition. The measurement of miR-1255b-5p in blood may provide a new noninvasive approach for the diagnosis of prostate cancer. miR-1255b-5p may become a potential therapeutic target for prostate cancer.
DOI: 10.6084/m9.figshare.17162471.v1
title: Diagnostic significance of microRNA-1255b-5p in prostate cancer patients and its effect on cancer cell function

description: Discerning between indolent and aggressive types is a big challenge of prostate cancer clinically to guide the adequate therapeutic regimen. We aimed to examine the relationship between miR-1255b-p expression and prostate cancer and elucidate the function of miR-1255b-5p in prostate cancer. miR-1255b-5p were measured using Quantitative Real-Time PCR from the blood 103 benign prostate hyperplasia (BPH) and 153 prostate cancer patients (117 indolent cases and 36 upgrading cases). Using receiver operating characteristic (ROC) curve analysis, the discriminating ability of miR-1255b-5p was accessed between BPH and prostate cancer participants, or indolent and aggressive type. Using CCK-8 and Transwell assays, the function of miR-1255b-5p on prostate cancer cells was investigated. The levels of miR-1255b-5p were significantly raised in prostate cancer patients when compared with BPH participants. MiR-1255b-5p level can distinguish prostate cancer patients from BPH or indolent type from aggressive type. Downregulation of miR-1255b-5p can suppress the proliferative, invasive, and migratory capacity, but this effect can be eradicated by <i>EPB41L1</i> inhibition. The measurement of miR-1255b-5p in blood may provide a new noninvasive approach for the diagnosis of prostate cancer. miR-1255b-5p may become a potential therapeutic target for prostate cancer.
DOI: 10.6084/m9.figshare.17122163
title: MicroRNA miR-145-5p regulates cell proliferation and cell migration in colon cancer by inhibiting chemokine (C-X-C motif) ligand 1 and integrin α2

description: Colon cancer (CC), which has high morbidity and mortality, can be regulated by microRNAs. This study aimed to investigate the regulatory function of microRNA miR-145-5p in CC cells. Bioinformatics analysis was used to screen key genes in CC. The expression of miR-145-5p, chemokine (C-X-C motif) ligand 1 (CXCL1), and integrin α2 (ITGA2) in CC was confirmed by quantitative reverse transcription polymerase chain reaction and western blotting. After cell transfection, changes in proliferation and migration in CC cells were detected using the cell counting kit-8 (CCK-8), colony formation assay, and wound healing assay. A luciferase assay was conducted to confirm the interactome of miR-145-5p, CXCL1, and ITGA2 in CC cells. Bioinformatics analysis confirmed that CXCL1 and ITGA2 were key genes in CC. After performing several cell functional experiments, the results confirmed that upregulation of miR-145-5p attenuated proliferation and migration of CC cells. Luciferase assay and western blotting confirmed that CXCL1 and ITGA2 were targets of miR-145-5p, and their expression in CC could be suppressed by miR-145-5p. In conclusion, miR-145-5p is a tumor suppressor in CC and can inhibit the expression of CXCL1 and ITGA2.
DOI: 10.6084/m9.figshare.17122163.v1
title: MicroRNA miR-145-5p regulates cell proliferation and cell migration in colon cancer by inhibiting chemokine (C-X-C motif) ligand 1 and integrin α2

description: Colon cancer (CC), which has high morbidity and mortality, can be regulated by microRNAs. This study aimed to investigate the regulatory function of microRNA miR-145-5p in CC cells. Bioinformatics analysis was used to screen key genes in CC. The expression of miR-145-5p, chemokine (C-X-C motif) ligand 1 (CXCL1), and integrin α2 (ITGA2) in CC was confirmed by quantitative reverse transcription polymerase chain reaction and western blotting. After cell transfection, changes in proliferation and migration in CC cells were detected using the cell counting kit-8 (CCK-8), colony formation assay, and wound healing assay. A luciferase assay was conducted to confirm the interactome of miR-145-5p, CXCL1, and ITGA2 in CC cells. Bioinformatics analysis confirmed that CXCL1 and ITGA2 were key genes in CC. After performing several cell functional experiments, the results confirmed that upregulation of miR-145-5p attenuated proliferation and migration of CC cells. Luciferase assay and western blotting confirmed that CXCL1 and ITGA2 were targets of miR-145-5p, and their expression in CC could be suppressed by miR-145-5p. In conclusion, miR-145-5p is a tumor suppressor in CC and can inhibit the expression of CXCL1 and ITGA2.
DOI: 10.34740/kaggle/dsv/7906669
title: Mahanagar Yatayat Transport Dataset
DOI: 10.6084/m9.figshare.17705559.v1
title: Long non-coding RNA DCST1-AS1/hsa-miR-582-5p/HMGB1 axis regulates colorectal cancer progression

description: Long non-coding RNAs (lncRNAs) are related to the initiation and progression of tumor and regulate various cellular processes including growth, invasion, migration, and apoptosis. Understanding the roles and mechanisms of lncRNAs in regulating cancer progression is crucial for formulating novel therapeutic strategies. Although lncRNA DCST1-antisense RNA 1(AS1) has been implicated in several cancers, its role in the progression of colorectal cancer (CRC) remains to be explored. This study focuses on elucidating the function of lncRNA DCST1-AS1 in CRC development and its underlying mechanism. We found that the expression of lncRNA DCST1-AS1 was up-regulated in CRC tissues and cell lines, and CRC patients with high lncRNA DCST1-AS1 expression were associated with a poor prognosis. Loss-of-function and gain-of-function experiment in CRC cell lines confirmed that lncRNA DCST1-AS1 promoted the malignant phenotype of CRC cells, including cell proliferation, colony formation, migration, and invasion. In addition, we identified the binding sites between lncRNA DCST1-AS1 and hsa-miR-582-5p, and between hsa-miR-582-5p and High Mobility Group Box 1 (HMGB1) through DIANA Tools and TargetScan database, which was further confirmed by dual-luciferase reporter assay. Functional assay further confirmed the crucial role of lncRNA DCST1-AS1/hsa-miR-582-5p/HMGB1 axis in modulating the malignant phenotype of CRC cells. Collectively, our data suggest that lncRNA DCST1-AS1 regulates the aggressiveness of CRC cells through hsa-miR-582-5p/HMGB1 axis. Our study provides novel insight into the mechanism of lncRNA DCST1-AS1 in CRC cells for targeted therapy.
DOI: 10.6084/m9.figshare.18134067.v1
title: N(6)-adenosine-methyltransferase-14 promotes glioma tumorigenesis by repressing argininosuccinate synthase 1 expression in an m6A-dependent manner

description: Glioma is one of the leading causes of tumor-related deaths worldwide, but its potential mechanism remains unclear. This study aimed to explore the biological role and potential mechanism of argininosuccinate synthase 1 (ASS1) in glioma. The relative expression levels of ASS1 in glioma specimens and cell lines were calculated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting. The biological functions of ASS1 were demonstrated using the 5-ethynyl-2ʹ-deoxyuridine (EdU) assay, transwell assay, and in vivo experiments. In addition, methylated RNA immunoprecipitation (MeRIP), RNA immunoprecipitation (RIP), and luciferase reporter assays were performed to explore the molecular mechanism of ASS1 in glioma. ASS1 expression levels were found to be downregulated in glioma specimens and cell lines. Functionally, we confirmed that ASS1 inhibited glioma cell proliferation, migration, invasion, and growth both. Furthermore, we found that ASS1 was a target of N(6)-adenosine-methyltransferase-14 (METTL14)-mediated N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) modification. Overexpression of METTL14 markedly elevated ASS1 mRNA m<sup>6</sup>A modification and suppressed ASS1 mRNA expression. We also revealed that METTL14-mediated ASS1 mRNA degradation relied on the YTH m6A RNA-binding protein 2 (YTHDF2)-dependent pathway. We confirmed that decreased ASS1 expression promoted the cell proliferation, migration, and invasion in glioma, and that the METTL14/ASS1/YTHDF2 regulatory axis may be an effective therapeutic target for glioma.
DOI: 10.5287/ora-exzbr0nny
title: Files associated with: "Investigations of electrophysiological mechanisms related to myocardial ischaemia in hypertrophic cardiomyopathy: implications for arrhythmic risk, ECG diagnosis, and antiarrhythmic therapy"

description: Contains meshes, MonoAlg3D source files and config files required to reproduce investigations in the DPhil thesis "Investigations of electrophysiological mechanisms related to myocardial ischaemia in hypertrophic cardiomyopathy: implications for arrhythmic risk, ECG diagnosis, and antiarrhythmic therapy".
DOI: 10.6084/m9.figshare.18134067.v2
title: RETRACTED ARTICLE: N(6)-adenosine-methyltransferase-14 promotes glioma tumorigenesis by repressing argininosuccinate synthase 1 expression in an m6A-dependent manner

description: The Publisher of the journal <i>Bioengineered</i>, have retracted the following article: Miao YQ, Chen W, Zhou J, Shen Q, Sun Y, Li T, Wang SC. N(6)-adenosine-methyltransferase-14 promotes glioma tumorigenesis by repressing argininosuccinate synthase 1 expression in an m6A-dependent manner. Bioengineered. 2022 Jan;13(1):1858-1871. doi: 10.1080/21655979.2021.2018386. Since publication, significant concerns have been raised about the compliance with ethical policies for human research and the integrity of the data reported in the article. When approached for an explanation, the authors provided some original data but were not able to provide all the necessary supporting information. As verifying the validity of published work is core to the scholarly record’s integrity, we are retracting the article. All authors listed in this publication have been informed. We have been informed in our decision-making by our editorial policies and the COPE guidelines. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as ‘Retracted.’
DOI: 10.6084/m9.figshare.17705559.v2
title: RETRACTED ARTICLE: Long non-coding RNA DCST1-AS1/hsa-miR-582-5p/HMGB1 axis regulates colorectal cancer progression

description: Long Huang, Gang Dai- 2022, Long non-coding RNA DCST1-AS1/hsa-miR-582-5p/HMGB1 axis regulates colorectal cancer progression, <i>Bioengineered</i> 13(1), doi: 10.1080/21655979.2021.1976894 Since publication, significant concerns have been raised about the integrity of the data and reported results in the article. When approached for an explanation, the authors did not respond, nor did they provide their original data or any necessary supporting information. As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article. All authors listed in this publication have been informed. We have been informed in our decision-making by our editorial policies and the COPE guidelines. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as ‘Retracted’.
DOI: 10.48597/4ur7-p4zh
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/fue4-m6u8
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/uuct-4dzz
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/dd95-h7jf
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/en9s-6ux6
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/ffzt-58xk
title: Measurement of Nitrogen_monoxide at Jungfraujoch

description: Measurement of Nitrogen_monoxide at Jungfraujoch
DOI: 10.48597/k993-2nu8
title: Measurement of Nitrogen_monoxide at Jungfraujoch

description: Measurement of Nitrogen_monoxide at Jungfraujoch
DOI: 10.48597/mvpx-d73c
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/p4ww-2qq3
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/vtgy-gxsc
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/zp34-wytm
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/zpdr-5vhh
title: Measurement of Nitrogen_monoxide at Jungfraujoch

description: Measurement of Nitrogen_monoxide at Jungfraujoch
DOI: 10.48597/5swd-r6gu
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/62aq-gcrk
title: Measurement of Nitrogen_monoxide at Jungfraujoch

description: Measurement of Nitrogen_monoxide at Jungfraujoch
DOI: 10.48597/au4n-zqez
title: Measurement of Nitrogen_monoxide at Jungfraujoch

description: Measurement of Nitrogen_monoxide at Jungfraujoch
DOI: 10.48597/epkr-e4cx
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/f6v4-ukx8
title: Measurement of Nitrogen_monoxide at Jungfraujoch

description: Measurement of Nitrogen_monoxide at Jungfraujoch
DOI: 10.48597/qpxs-zzf3
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/rnsb-j679
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/s6ss-f2fy
title: Measurement of Nitrogen_monoxide at Jungfraujoch

description: Measurement of Nitrogen_monoxide at Jungfraujoch
DOI: 10.48597/vmgu-wgj8
title: Measurement of Nitrogen_monoxide at Jungfraujoch

description: Measurement of Nitrogen_monoxide at Jungfraujoch
DOI: 10.48597/wpwc-z7tw
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/znzx-v7ys
title: Measurement of Nitrogen_dioxide at Jungfraujoch

description: Measurement of Nitrogen_dioxide at Jungfraujoch
DOI: 10.48597/9krm-pkxj
title: Measurement of Nitrogen_monoxide at Jungfraujoch

description: Measurement of Nitrogen_monoxide at Jungfraujoch
DOI: 10.48597/qfwj-z82x
title: Measurement of Nitrogen_monoxide at Jungfraujoch

description: Measurement of Nitrogen_monoxide at Jungfraujoch
DOI: 10.5287/ora-jvgnk4rzg
title: Wave mechanics in an ionic liquid mixture (data)

description: Measurements of interaction free energies across ionic liquid mixtures as discussed and analysed in the associated manuscript
DOI: 10.5281/zenodo.10849559
title: Impact of Digital Inclusive Finance on Agricultural Total Factor Productivity in Zhejiang Province from the Perspective of Integrated Development of Rural Industries
DOI: 10.5281/zenodo.10849560
title: Impact of Digital Inclusive Finance on Agricultural Total Factor Productivity in Zhejiang Province from the Perspective of Integrated Development of Rural Industries
DOI: 10.18112/openneuro.ds005038.v1.0.1
title: Modality-based Multitasking, practice data
DOI: 10.6084/m9.figshare.25451866
title: pulmonaryAirwayWeights.h5

description: lung weights airways<br>
DOI: 10.6084/m9.figshare.25451866.v1
title: pulmonaryAirwayWeights.h5

description: lung weights airways<br>
DOI: 10.6084/m9.figshare.25451866.v2
title: pulmonaryAirwayWeights.h5

description: lung weights airways<br>
DOI: 10.6084/m9.figshare.17185702
title: Exosomal microRNA-150-5p from bone marrow mesenchymal stromal cells mitigates cerebral ischemia/reperfusion injury via targeting toll-like receptor 5

description: MicroRNA (miR)-150-5p has been investigated in many studies, while the role of exosomal miR-150-5p from bone arrow mesenchymal stromal cells (BMSCs) on cerebral ischemia/reperfusion (I/R) injury is not fully explored. This research aims to probe the effects of exosomal miR-150-5p from BMSCs on cerebral I/R injury via regulating B-cell translocation gene 2 (TLR5). Bone marrow mesenchymal stem cell-derived exosomes (BMSCs-Exo) were isolated and identified. The middle cerebral artery occlusion (MCAO) rat model was established and treated by BMSCs-Exo. Then, functional assays were conducted to explore neurological function, pathological changes, neuron apoptosis and inflammatory factors in MCAO rats. miR-150-5p and TLR5 expression in rat brain tissues were detected. Then, gain and loss-function assays were conducted to determine the impact of exosomes, miR-150-5p and TLR5 on neurological function, pathological changes, neuron apoptosis and inflammatory factors of MCAO rats. The binding relation between miR-150-5p and TLR5 was validated. It was found that miR-150-5p expression was decreased while TLR5 level was augmented in MCAO rats. BMSCs-Exo could improve neurological function, pathological changes, decelerate neuron apoptosis and reduce inflammatory factors in MCAO rats. Enriched miR-150-5pcould enhance the protective effects of BMSCs-Exo on cerebral I/R injury. The elevated TLR5 reversed the impacts of elevated exosomal miR-150-5p on cerebral I/R injury. TLR5 was targeted by miR-150-5p. This research manifested that exosomal miR-150-5p from BMSCs exerts protective effects on cerebral I/R injury via repressing TLR5. This study provided novel therapeutic targets for the treatment of cerebral I/R injury.
DOI: 10.6084/m9.figshare.17185702.v2
title: Exosomal microRNA-150-5p from bone marrow mesenchymal stromal cells mitigates cerebral ischemia/reperfusion injury via targeting toll-like receptor 5

description: MicroRNA (miR)-150-5p has been investigated in many studies, while the role of exosomal miR-150-5p from bone arrow mesenchymal stromal cells (BMSCs) on cerebral ischemia/reperfusion (I/R) injury is not fully explored. This research aims to probe the effects of exosomal miR-150-5p from BMSCs on cerebral I/R injury via regulating B-cell translocation gene 2 (TLR5). Bone marrow mesenchymal stem cell-derived exosomes (BMSCs-Exo) were isolated and identified. The middle cerebral artery occlusion (MCAO) rat model was established and treated by BMSCs-Exo. Then, functional assays were conducted to explore neurological function, pathological changes, neuron apoptosis and inflammatory factors in MCAO rats. miR-150-5p and TLR5 expression in rat brain tissues were detected. Then, gain and loss-function assays were conducted to determine the impact of exosomes, miR-150-5p and TLR5 on neurological function, pathological changes, neuron apoptosis and inflammatory factors of MCAO rats. The binding relation between miR-150-5p and TLR5 was validated. It was found that miR-150-5p expression was decreased while TLR5 level was augmented in MCAO rats. BMSCs-Exo could improve neurological function, pathological changes, decelerate neuron apoptosis and reduce inflammatory factors in MCAO rats. Enriched miR-150-5pcould enhance the protective effects of BMSCs-Exo on cerebral I/R injury. The elevated TLR5 reversed the impacts of elevated exosomal miR-150-5p on cerebral I/R injury. TLR5 was targeted by miR-150-5p. This research manifested that exosomal miR-150-5p from BMSCs exerts protective effects on cerebral I/R injury via repressing TLR5. This study provided novel therapeutic targets for the treatment of cerebral I/R injury.
DOI: 10.6084/m9.figshare.17185702.v1
title: Exosomal microRNA-150-5p from bone marrow mesenchymal stromal cells mitigates cerebral ischemia/reperfusion injury via targeting toll-like receptor 5

description: MicroRNA (miR)-150-5p has been investigated in many studies, while the role of exosomal miR-150-5p from bone marrow mesenchymal stromal cells (BMSCs) on cerebral ischemia/reperfusion (I/R) injury is not fully explored. This research aims to probe the effects of exosomal miR-150-5p from BMSCs on cerebral I/R injury via regulating B-cell translocation gene 2 (TLR5). BMSCs were cultured and transfected with miR-150-5p mimic, then exosomes from BMSCs were extracted. The middle cerebral artery occlusion (MCAO) rat model was established, and miR-150-5p and TLR5 levels in rat brain tissues were detected. Then, gain and loss-function assays were conducted to determine the impact of exosomes, miR-150-5p and TLR5 on neurological function, pathological changes, neuron apoptosis and inflammatory factors of MCAO rats. The binding relation between miR-150-5p and TLR5 was validated. It was found that miR-150-5p expression was decreased while TLR5 level was augmented in MCAO rats. The exosomes from BMSCs could improve neurological function, pathological changes, decelerate neuron apoptosis and reduce inflammatory factors in MCAO rats. Enriched miR-150-5p or decreased TLR5 could enhance the protective effects of exosomes from BMSCs on cerebral I/R injury. The elevated TLR5 reversed the impacts of elevated exosomal miR-150-5p. TLR5 was targeted by miR-150-5p. This research manifested that exosomal miR-150-5p from BMSCs exerts protective effects on cerebral I/R injury via repressing TLR5. This study provided novel therapeutic targets for the treatment of cerebral I/R injury.