cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.19336763
title: Long noncoding RNA LINC01426 promotes the progression of lung adenocarcinoma via regulating miRNA-125a-5p/ casein kinase 2 alpha 1 axis

description: Although long noncoding RNAs (lncRNAs) in lung adenocarcinoma (LUAD) have been increasingly studied, LINC01426 has not been fully investigated in LUAD. The GEPIA database revealed that LINC01426 was upregulated in LUAD tissues. In our study, we further verified the significantly high expression of LINC01426 in LUAD tissues and cell lines. We also analyzed the LINC01426 expression level and LUAD clinical features and found that high LINC01426 expression was associated with tumor diameter; tumor, node, and metastases (TNM) staging; lymph node metastasis (LNM); and overall survival (OS) rate of LUAD patients. In vitro experiments revealed that suppression of LINC01426 could repress the proliferation, migration and invasion of LUAD cells. Then, the bioinformatic analysis revealed that there were binding domains between miR-125a-5p and the 3′-UTR of LINC01426. As revealed by dual-luciferase reporter gene experiment and RNA Binding Protein Immunoprecipitation (RIP) assay, miR-125a-5p could bind to LINC01426. Additionally, the results of qRT-PCR and Pearson’s analysis respectively revealed that miR-125a-5p was slightly expressed in LUAD and its expression was negatively correlated with LINC01426. Moreover, casein kinase 2 alpha 1 (CSNK2A1) was predicted to bind to miR-125a-5p. CSNK2A1 expression was remarkably high in LUAD tissues, negatively associated with miR-125a-5p, and positively correlated with LINC01426. Subsequently, our results showed that CSNK2A1 enhanced the malignant progression of LUAD cells. Overall, our study revealed that LINC01426 might regulate the malignant phenotype of LUAD via the miR-125a-5p/CSNK2A1 axis.
DOI: 10.6084/m9.figshare.19336763.v1
title: Long noncoding RNA LINC01426 promotes the progression of lung adenocarcinoma via regulating miRNA-125a-5p/ casein kinase 2 alpha 1 axis

description: Although long noncoding RNAs (lncRNAs) in lung adenocarcinoma (LUAD) have been increasingly studied, LINC01426 has not been fully investigated in LUAD. The GEPIA database revealed that LINC01426 was upregulated in LUAD tissues. In our study, we further verified the significantly high expression of LINC01426 in LUAD tissues and cell lines. We also analyzed the LINC01426 expression level and LUAD clinical features and found that high LINC01426 expression was associated with tumor diameter; tumor, node, and metastases (TNM) staging; lymph node metastasis (LNM); and overall survival (OS) rate of LUAD patients. In vitro experiments revealed that suppression of LINC01426 could repress the proliferation, migration and invasion of LUAD cells. Then, the bioinformatic analysis revealed that there were binding domains between miR-125a-5p and the 3′-UTR of LINC01426. As revealed by dual-luciferase reporter gene experiment and RNA Binding Protein Immunoprecipitation (RIP) assay, miR-125a-5p could bind to LINC01426. Additionally, the results of qRT-PCR and Pearson’s analysis respectively revealed that miR-125a-5p was slightly expressed in LUAD and its expression was negatively correlated with LINC01426. Moreover, casein kinase 2 alpha 1 (CSNK2A1) was predicted to bind to miR-125a-5p. CSNK2A1 expression was remarkably high in LUAD tissues, negatively associated with miR-125a-5p, and positively correlated with LINC01426. Subsequently, our results showed that CSNK2A1 enhanced the malignant progression of LUAD cells. Overall, our study revealed that LINC01426 might regulate the malignant phenotype of LUAD via the miR-125a-5p/CSNK2A1 axis.
DOI: 10.6084/m9.figshare.19209416
title: A peptide derived from the N-terminus of charged multivesicular body protein 6 (CHMP6) promotes the secretion of gene editing proteins via small extracellular vesicle production

description: Extracellular vesicles (EVs) are a promising new therapeutic platform. However, the low cargo-loading efficiency limits their clinical translation. In this study, we developed a high-yield EV cargo-loading device and explored its ability to encapsulate gene editing proteins. A series of fusion protein-based systems were constructed and their cargo loading efficiencies were compared by a NanoGlo luciferase assay. A myristoylated (Myr) peptide tag cloned from the N-terminal region of charged multivesicular body protein 6 (CHMP6), termed Myr(CHMP6), outcompeted CD9, ARRDC1, and other short polypeptides as an active packaging device. As determined by nanoparticle tracking analysis and transmission electron microscopy, the overexpression of Myr(CHMP6) increased small EV (sEV) production in Lenti-X 293T  cells without altering sEV morphology. The high passive packaging efficiency of Myr(CHMP6) was also elucidated for unmodified cargo loading. Western blotting revealed that Myr(CHMP6) facilitated the loading of Cre and Cas9 into sEVs without the generation of packaging device-cargo fusion proteins. Furthermore, Myr(CHMP6)-modified sEVs loaded with Cre or Cas9 promoted gene-editing in recipient cells, as observed using a fluorescence reporter system. Subsequent investigation demonstrated a dose-dependent effect of Myr(CHMP6) tag-induced cargo-loading. Mechanistically, N-myristoylation alone was necessary but not sufficient for the effective packaging of proteins into EVs. Thus, our results indicated that Myr(CHMP6) induces sEV production and may be effective in loading gene editing proteins into sEVs for therapeutic purposes.
DOI: 10.6084/m9.figshare.19209416.v1
title: A peptide derived from the N-terminus of charged multivesicular body protein 6 (CHMP6) promotes the secretion of gene editing proteins via small extracellular vesicle production

description: Extracellular vesicles (EVs) are a promising new therapeutic platform. However, the low cargo-loading efficiency limits their clinical translation. In this study, we developed a high-yield EV cargo-loading device and explored its ability to encapsulate gene editing proteins. A series of fusion protein-based systems were constructed and their cargo loading efficiencies were compared by a NanoGlo luciferase assay. A myristoylated (Myr) peptide tag cloned from the N-terminal region of charged multivesicular body protein 6 (CHMP6), termed Myr(CHMP6), outcompeted CD9, ARRDC1, and other short polypeptides as an active packaging device. As determined by nanoparticle tracking analysis and transmission electron microscopy, the overexpression of Myr(CHMP6) increased small EV (sEV) production in Lenti-X 293T  cells without altering sEV morphology. The high passive packaging efficiency of Myr(CHMP6) was also elucidated for unmodified cargo loading. Western blotting revealed that Myr(CHMP6) facilitated the loading of Cre and Cas9 into sEVs without the generation of packaging device-cargo fusion proteins. Furthermore, Myr(CHMP6)-modified sEVs loaded with Cre or Cas9 promoted gene-editing in recipient cells, as observed using a fluorescence reporter system. Subsequent investigation demonstrated a dose-dependent effect of Myr(CHMP6) tag-induced cargo-loading. Mechanistically, N-myristoylation alone was necessary but not sufficient for the effective packaging of proteins into EVs. Thus, our results indicated that Myr(CHMP6) induces sEV production and may be effective in loading gene editing proteins into sEVs for therapeutic purposes.
DOI: 10.6084/m9.figshare.19195396
title: MYB proto-oncogene like 2 promotes hepatocellular carcinoma growth and glycolysis via binding to the <i>Optic atrophy 3</i> promoter and activating its expression

description: Optic atrophy 3 (OPA3) is an integral protein of the mitochondrial outer membrane. The current study explored the expression of <i>OPA3</i> in hepatocellular carcinoma (HCC), its association with the prognosis and its involvement in HCC cell proliferation and aerobic glycolysis. In addition, the transcription factors that activate its expression were screened and validated. Gene expression data in normal liver and liver cancer were acquired from the Genotype-Tissue Expression Project (GTEx) and The Cancer Genome Atlas (TCGA)-Liver Hepatocellular Carcinoma (TCGA-LIHC). Chromatin immunoprecipitation-seq data (GSM1010876) in Cistrome Data Browser was used for searching transcriptional factors binding to the <i>OPA3</i> promoter. HCC cell lines HLF and JHH2 were used for <i>in-vitro</i> and <i>in-vivo</i> studies. Results showed that <i>OPA3</i> is significantly upregulated in HCC and associated with unfavorable prognosis. <i>OPA3</i> knockdown impaired HCC cell growth <i>in vitro</i> and <i>in vivo</i>. Besides, it decreased glucose uptake, lactate production, intracellular ATP levels, and extracellular acidification rate (ECAR) of HLF and JHH2 cells. MYB Proto-Oncogene Like 2 (MYBL2) can bind to the promoter of <i>OPA3</i> and enhance its transcription. <i>MYBL2</i> knockdown decreased aerobic glycolysis in HCC cells. <i>OPA3</i> overexpression reversed these alterations. In conclusion, this study revealed a novel MYBL2-OPA3 axis that enhances HCC cell proliferation and aerobic glycolysis.
DOI: 10.6084/m9.figshare.19195396.v1
title: MYB proto-oncogene like 2 promotes hepatocellular carcinoma growth and glycolysis via binding to the <i>Optic atrophy 3</i> promoter and activating its expression

description: Optic atrophy 3 (OPA3) is an integral protein of the mitochondrial outer membrane. The current study explored the expression of <i>OPA3</i> in hepatocellular carcinoma (HCC), its association with the prognosis and its involvement in HCC cell proliferation and aerobic glycolysis. In addition, the transcription factors that activate its expression were screened and validated. Gene expression data in normal liver and liver cancer were acquired from the Genotype-Tissue Expression Project (GTEx) and The Cancer Genome Atlas (TCGA)-Liver Hepatocellular Carcinoma (TCGA-LIHC). Chromatin immunoprecipitation-seq data (GSM1010876) in Cistrome Data Browser was used for searching transcriptional factors binding to the <i>OPA3</i> promoter. HCC cell lines HLF and JHH2 were used for <i>in-vitro</i> and <i>in-vivo</i> studies. Results showed that <i>OPA3</i> is significantly upregulated in HCC and associated with unfavorable prognosis. <i>OPA3</i> knockdown impaired HCC cell growth <i>in vitro</i> and <i>in vivo</i>. Besides, it decreased glucose uptake, lactate production, intracellular ATP levels, and extracellular acidification rate (ECAR) of HLF and JHH2 cells. MYB Proto-Oncogene Like 2 (MYBL2) can bind to the promoter of <i>OPA3</i> and enhance its transcription. <i>MYBL2</i> knockdown decreased aerobic glycolysis in HCC cells. <i>OPA3</i> overexpression reversed these alterations. In conclusion, this study revealed a novel MYBL2-OPA3 axis that enhances HCC cell proliferation and aerobic glycolysis.
DOI: 10.6084/m9.figshare.19334999
title: Circular RNA coiled-coil domain containing 66 regulates malignant development of papillary thyroid carcinoma by upregulating La ribonucleoprotein 1 <i>via</i> the sponge effect on miR-129-5p

description: Circular RNAs (circRNAs) play vital roles in the development and progression of various diseases. CircRNA coiled-coil domain containing 66 (circ-CCDC66) has been reported to be involved in several cancers, but its biological function and underlying mechanism in papillary thyroid carcinoma (PTC) remain unclear. We detected the relative expression level of circ-CCDC66 in PTC specimens and cell lines using real-time reverse transcription PCR. In addition, EdU assay, transwell assay, and xenograft analysis were performed to measure the effect of circ-CCDC66 on the proliferative, migratory, and invasive capacities of PTC cells. We also investigated the potential mechanism of circ-CCDC66 by bioinformatics analysis, RNA immunoprecipitation, and dual-luciferase reporter assay. We observed that circ-CCDC66 expression was upregulated in PTC specimens and cell lines and was correlated with poor clinical characteristics of PTC patients. Moreover, <i>in vitro</i> experiments demonstrated that knockdown of circ-CCDC66 markedly suppressed the proliferative, migratory, and invasive capacities of PTC cells. Mechanistically, miR-129-5p was a target gene of circ-CCDC66 and was downregulated in PTC tissues. LARP1, a downstream target of miR-129-5p, was upregulated in PTC tissues. In addition, we confirmed that inhibition of circ-CCDC66 could repress xenograft tumor growth. Circ-CCDC66 promoted PTC proliferation, migration, invasion, and tumor growth by sponging miR-129-5p and promoting LARP1 expression.
DOI: 10.6084/m9.figshare.19334999.v1
title: Circular RNA coiled-coil domain containing 66 regulates malignant development of papillary thyroid carcinoma by upregulating La ribonucleoprotein 1 <i>via</i> the sponge effect on miR-129-5p

description: Circular RNAs (circRNAs) play vital roles in the development and progression of various diseases. CircRNA coiled-coil domain containing 66 (circ-CCDC66) has been reported to be involved in several cancers, but its biological function and underlying mechanism in papillary thyroid carcinoma (PTC) remain unclear. We detected the relative expression level of circ-CCDC66 in PTC specimens and cell lines using real-time reverse transcription PCR. In addition, EdU assay, transwell assay, and xenograft analysis were performed to measure the effect of circ-CCDC66 on the proliferative, migratory, and invasive capacities of PTC cells. We also investigated the potential mechanism of circ-CCDC66 by bioinformatics analysis, RNA immunoprecipitation, and dual-luciferase reporter assay. We observed that circ-CCDC66 expression was upregulated in PTC specimens and cell lines and was correlated with poor clinical characteristics of PTC patients. Moreover, <i>in vitro</i> experiments demonstrated that knockdown of circ-CCDC66 markedly suppressed the proliferative, migratory, and invasive capacities of PTC cells. Mechanistically, miR-129-5p was a target gene of circ-CCDC66 and was downregulated in PTC tissues. LARP1, a downstream target of miR-129-5p, was upregulated in PTC tissues. In addition, we confirmed that inhibition of circ-CCDC66 could repress xenograft tumor growth. Circ-CCDC66 promoted PTC proliferation, migration, invasion, and tumor growth by sponging miR-129-5p and promoting LARP1 expression.
DOI: 10.6084/m9.figshare.19336398
title: Leucine rich alpha-2-glycoprotein 1 (Lrg1) silencing protects against sepsis-mediated brain injury by inhibiting transforming growth factor beta1 (TGFβ1)/SMAD signaling pathway

description: Sepsis-associated encephalopathy (SAE) is key manifestation of sepsis which is responsible for increased morbidity and mortality. Leucine rich alpha-2-glycoprotein 1 (Lrg1) is a secreted protein implicated in a variety of diseases. We aimed to explore the effects and potential mechanism of Lrg1 on sepsis-mediated brain injury. A sepsis-induced brain damage mice model was established. Then, ELISA was utilized to detect the levels of inflammatory factors in brain tissues. Behavioral performance, spatial learning and memory of mice were evaluated by open field test and Morris water maze test. The number of neurons was tested by H&E staining. Lrg1 expression was evaluated by RT-qPCR and western blot. In vitro, mouse hippocampal neuronal cell line (HT22) was stimulated by lipopolysaccharide (LPS). After Lrg1 silencing, cell viability was determined using CCK-8 and cell apoptosis was assessed by TUNEL. The levels of inflammatory factors were detected by ELISA. Moreover, western blot was applied to analyze the expression of proteins in transforming growth factor beta1 (TGFβ1)/SMAD signaling. Results revealed that mice in the model group showed obvious behavioral changes. Lrg1 was highly expressed in the brain tissues of model mice. Besides, Lrg1 knockdown suppressed the inflammation and apoptosis of LPS-induced HT22 cells. Moreover, Lrg1 silencing caused the inactivation of TGFβ1/SMAD signaling. Rescue assays confirmed that TGFβ1 overexpression reversed the impacts of Lrg1 deletion on the inflammation and apoptosis in LPS-induced HT22 cells. Collectively, Lrg1 silencing alleviates brain injury in SAE via inhibiting TGFβ1/SMAD signaling, implying that Lrg1 might serve as a promising target for SAE treatment.
DOI: 10.6084/m9.figshare.19336398.v1
title: Leucine rich alpha-2-glycoprotein 1 (Lrg1) silencing protects against sepsis-mediated brain injury by inhibiting transforming growth factor beta1 (TGFβ1)/SMAD signaling pathway

description: Sepsis-associated encephalopathy (SAE) is key manifestation of sepsis which is responsible for increased morbidity and mortality. Leucine rich alpha-2-glycoprotein 1 (Lrg1) is a secreted protein implicated in a variety of diseases. We aimed to explore the effects and potential mechanism of Lrg1 on sepsis-mediated brain injury. A sepsis-induced brain damage mice model was established. Then, ELISA was utilized to detect the levels of inflammatory factors in brain tissues. Behavioral performance, spatial learning and memory of mice were evaluated by open field test and Morris water maze test. The number of neurons was tested by H&E staining. Lrg1 expression was evaluated by RT-qPCR and western blot. In vitro, mouse hippocampal neuronal cell line (HT22) was stimulated by lipopolysaccharide (LPS). After Lrg1 silencing, cell viability was determined using CCK-8 and cell apoptosis was assessed by TUNEL. The levels of inflammatory factors were detected by ELISA. Moreover, western blot was applied to analyze the expression of proteins in transforming growth factor beta1 (TGFβ1)/SMAD signaling. Results revealed that mice in the model group showed obvious behavioral changes. Lrg1 was highly expressed in the brain tissues of model mice. Besides, Lrg1 knockdown suppressed the inflammation and apoptosis of LPS-induced HT22 cells. Moreover, Lrg1 silencing caused the inactivation of TGFβ1/SMAD signaling. Rescue assays confirmed that TGFβ1 overexpression reversed the impacts of Lrg1 deletion on the inflammation and apoptosis in LPS-induced HT22 cells. Collectively, Lrg1 silencing alleviates brain injury in SAE via inhibiting TGFβ1/SMAD signaling, implying that Lrg1 might serve as a promising target for SAE treatment.
DOI: 10.15468/dl.wwfz9c
title: Occurrence Download

description: A dataset containing 88 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Amolops lifanensis"
 ]
}

 The dataset includes 88 records from 5 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0030116-250920141307145/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.19338092
title: P53 and taurine upregulated gene 1 promotes the repair of the DeoxyriboNucleic Acid damage induced by bupivacaine in murine primary sensory neurons

description: The research aimed to explore the biological role of p53 protein and long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in bupivacaine (bup)-induced neurotoxicity. Our work treated dorsal root ganglion (DRG) cells with bup, detected cell viability through CCK-8, apoptosis through TUNEL assays, DeoxyriboNucleic Acid (DNA) damage through γ-H2AX protein and comet assay, including p53 mRNA, protein and TUG1 expression through q-PCR and western blot, furthermore, cell viability and DNA damage were determined after the silencing of p53 and TUG1, biological information and TUG1 FISH combined with p53 protein immunofluorescence (IF) was performed to determine the cellular localization of these molecule. <i>In vivo</i> experiments, we explored the impact of intrathecal injection of bup on p53 mRNA and protein, TUG1, γ-H2AX protein expression. The results showed that bup was available to signally decreased cell viability, promoted apoptosis rate and DNA damage, additionally, bup increased p53 mRNA and protein and TUG1 expression. P53 siRNA and TUG1 siRNA significantly increased DNA damage. Furthermore, bioinformatics analysis and colocalization experiments revealed that the p53 protein is a transcription factor of TUG1, in vivo experiment, intrathecal injection of bup increased the p53 mRNA, p53 protein, TUG1 and γ-H2AX protein in the murine DRG. In this study, it was found p53 and TUG1 promote the repair of the DNA damage induced by bup in murine dorsal root ganglion cells, suggesting a new strategy for the amelioration of bup-induced neurotoxicity.
DOI: 10.6084/m9.figshare.19338092.v1
title: P53 and taurine upregulated gene 1 promotes the repair of the DeoxyriboNucleic Acid damage induced by bupivacaine in murine primary sensory neurons

description: The research aimed to explore the biological role of p53 protein and long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in bupivacaine (bup)-induced neurotoxicity. Our work treated dorsal root ganglion (DRG) cells with bup, detected cell viability through CCK-8, apoptosis through TUNEL assays, DeoxyriboNucleic Acid (DNA) damage through γ-H2AX protein and comet assay, including p53 mRNA, protein and TUG1 expression through q-PCR and western blot, furthermore, cell viability and DNA damage were determined after the silencing of p53 and TUG1, biological information and TUG1 FISH combined with p53 protein immunofluorescence (IF) was performed to determine the cellular localization of these molecule. <i>In vivo</i> experiments, we explored the impact of intrathecal injection of bup on p53 mRNA and protein, TUG1, γ-H2AX protein expression. The results showed that bup was available to signally decreased cell viability, promoted apoptosis rate and DNA damage, additionally, bup increased p53 mRNA and protein and TUG1 expression. P53 siRNA and TUG1 siRNA significantly increased DNA damage. Furthermore, bioinformatics analysis and colocalization experiments revealed that the p53 protein is a transcription factor of TUG1, in vivo experiment, intrathecal injection of bup increased the p53 mRNA, p53 protein, TUG1 and γ-H2AX protein in the murine DRG. In this study, it was found p53 and TUG1 promote the repair of the DNA damage induced by bup in murine dorsal root ganglion cells, suggesting a new strategy for the amelioration of bup-induced neurotoxicity.
DOI: 10.6084/m9.figshare.19195371
title: Down-regulated long non-coding RNA LHFPL3 antisense RNA 1 inhibits the radiotherapy resistance of nasopharyngeal carcinoma via modulating microRNA-143-5p/homeobox A6 axis

description: The function of long non-coding RNA LHFPL3 antisense RNA 1 (LHFPL3-AS1) in cancer progression has been studied, while its role in nasopharyngeal carcinoma (NPC) remains unclear. This study aims to unravel the effects of LHFPL3-AS1 on NPC progression via microRNA (miR)-143-5p/homeobox A6 (HOXA6) axis. NPC tissues were collected and NPC cells were cultured. NPC cells were subjected to radiation therapy to construct the radiation therapy resistance NPC cell line. The levels of LHFPL3-AS1, miR-143-5p and HOXA6 in NPC cells and tissues were examined. LHFPL3-AS1, miR-143-5p or HOXA6 expression was changed and then transfected into radiation-resistant NPC cells to detect cell proliferation, colony formation, migration, invasion and cell apoptosis <i>in vitro</i>. The tumorigenesis in nude mice <i>in vivo</i> was conducted to detect tumor growth. The targeting relations among LHFPL3-AS1, miR-143-5p and HOXA6 were validated. It was discovered that LHFPL3-AS1 and HOXA6 expression was elevated while the miR-143-5p level was depleted in radiation-resistant NPC cells and NPC tissues. The silenced LHFPL3-AS1 or augmented miR-143-5p repressed the proliferation, colony formation, migration and invasion of radiation-resistant NPC cells, while accelerated cell apoptosis <i>in vitro</i>. Silenced LHFPL3-AS1 hindered tumor growth <i>in vivo</i>. MiR-143-5p deletion reversed the effects of reduced LHFPL3-AS1; while HOXA6 upregulation reversed the effects of enriched miR-143-5p. LHFPL3-AS1 sponged miR-143-5p that targeted HOXA6. It is concluded that the down-regulated LHFPL3-AS1 retards the development of radiation-resistant NPC cells via sponging miR-143-5p to modulate HOXA6. This study reveals novel therapeutic targets for NPC treatment.