cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.19166110
title: LncRNA LINC01315 silencing modulates cancer stem cell properties and epithelial-to-mesenchymal transition in colorectal cancer via miR-484/DLK1 axis

description: Long non-coding RNA long intergenic non-protein coding RNA 01315 (LncRNA LINC01315) has been found to be implicated in various cancers, but its role and functions in colorectal cancer (CRC) remain to be addressed. Data on LINC01315 expression in CRC were gathered using bioinformatics analysis, and cancer stem cells (CSCs) were sorted by aldehyde dehydrogenase (ALDH) assay and flow cytometry. Migration, invasion, and stemness of CSCs isolated from CRC cells after transfection were determined by scratch, Transwell, and sphere-formation assays, respectively. Tumor xenograft model was constructed. Target genes and potential-binding sites were predicted using online databases and further confirmed via dual-luciferase reporter assay. Relative factors expressions were determined via quantitative real-time polymerase-chain reaction and Western blot as needed. LINC01315 was high-expressed in CRC and ALDH<sup>+</sup> cells. LINC01315 silencing suppressed the migration, invasion, and sphere formation of CRC cells and tumor growth, and downregulated expressions of CSC molecules (ALDH, cluster of difference 44 (CD44), Prominin, and sex determining region Y-box 2 (SOX2)), Zinc Finger E-Box Binding Homeobox 1 (ZEB1) and Vimentin but upregulated E-Cadherin expression. MiR-484 could competitively bind with LINC01315, and LINC01315 silencing promoted miR-484 expression. The level of Delta Like Non-Canonical Notch Ligand 1 (DLK1), the target gene of miR-484, was enhanced by overexpressed LINC01315 yet was suppressed by LINC01315 silencing. Also, DLK1 silencing reversed the effects of downregulated miR-484 on migration, invasion, sphere formation, and CSC molecules expressions in CRC cells. LINC01315 silencing modulated CSC properties and epithelial-to-mesenchymal transition via miR-484/DLK1 axis.
DOI: 10.6084/m9.figshare.19166110.v1
title: LncRNA LINC01315 silencing modulates cancer stem cell properties and epithelial-to-mesenchymal transition in colorectal cancer via miR-484/DLK1 axis

description: Long non-coding RNA long intergenic non-protein coding RNA 01315 (LncRNA LINC01315) has been found to be implicated in various cancers, but its role and functions in colorectal cancer (CRC) remain to be addressed. Data on LINC01315 expression in CRC were gathered using bioinformatics analysis, and cancer stem cells (CSCs) were sorted by aldehyde dehydrogenase (ALDH) assay and flow cytometry. Migration, invasion, and stemness of CSCs isolated from CRC cells after transfection were determined by scratch, Transwell, and sphere-formation assays, respectively. Tumor xenograft model was constructed. Target genes and potential-binding sites were predicted using online databases and further confirmed via dual-luciferase reporter assay. Relative factors expressions were determined via quantitative real-time polymerase-chain reaction and Western blot as needed. LINC01315 was high-expressed in CRC and ALDH<sup>+</sup> cells. LINC01315 silencing suppressed the migration, invasion, and sphere formation of CRC cells and tumor growth, and downregulated expressions of CSC molecules (ALDH, cluster of difference 44 (CD44), Prominin, and sex determining region Y-box 2 (SOX2)), Zinc Finger E-Box Binding Homeobox 1 (ZEB1) and Vimentin but upregulated E-Cadherin expression. MiR-484 could competitively bind with LINC01315, and LINC01315 silencing promoted miR-484 expression. The level of Delta Like Non-Canonical Notch Ligand 1 (DLK1), the target gene of miR-484, was enhanced by overexpressed LINC01315 yet was suppressed by LINC01315 silencing. Also, DLK1 silencing reversed the effects of downregulated miR-484 on migration, invasion, sphere formation, and CSC molecules expressions in CRC cells. LINC01315 silencing modulated CSC properties and epithelial-to-mesenchymal transition via miR-484/DLK1 axis.
DOI: 10.6084/m9.figshare.17213003.v1
title: Monoclonal antibodies to activated CDK4: use to investigate normal and cancerous cell cycle regulation and involvement of phosphorylations of p21 and p27

description: Cyclin-dependent kinase 4 (CDK4) is a master integrator that couples mitogenic/oncogenic signaling with the cell division cycle. It is deregulated in most cancers and inhibitors of CDK4 have become standard of care drugs for metastatic estrogen-receptor positive breast cancers and are being evaluated in a variety of other cancers. We previously characterized the T-loop phosphorylation at T172 of CDK4 as the highly regulated step that determines the activity of cyclin D-CDK4 complexes. Moreover we demonstrated that the highly variable detection of T172-phosphorylated CDK4 signals the presence or absence of the active CDK4 targeted by the CDK4/6 inhibitory drugs, which predicts the tumor cell sensitivity to these drugs including palbociclib. To date, the phosphorylation of CDK4 has been very poorly studied because only few biochemical techniques and reagents are available for it. In addition, the available ones including 2D-IEF separation of CDK4 modified forms are considered too tedious. The present report describes the generation, selection and characterization of the first monoclonal antibodies that specifically recognize the active CDK4 phosphorylated on its T172 residue. One key to this success was the immunization with a long phosphopeptide corresponding to the complete activation segment of CDK4. These monoclonal antibodies specifically recognize T172-phosphorylated CDK4 in a variety of assays, including western blotting, immunoprecipitation and, as a capture antibody, a sensitive ELISA from cell lysates. The specific immunoprecipitation of T172-phosphorylated CDK4 allowed to clarify the involvement of phosphorylations of co-immunoprecipitated p21 and p27, showing a privileged interaction of T172-phosphorylated CDK4 with S130-phosphorylated p21 and S10-phosphorylated p27.
 <b>Abbreviations</b>:
2D: two-dimensional; CAK: CDK-activating kinase; CDK: cyclin-dependent kinase; HAT: Hypoxanthine-Aminopterin-Thymidine; FBS: fetal bovine serum; IP: immunoprecipitation; ID: immunodetection; mAb: monoclonal antibody; PAGE: polyacrylamide gel electrophoresis; PBS: phosphate buffer saline; pRb: retinoblastoma susceptibility protein; SDS: sodium dodecyl sulfate; DTT: dithiotreitol; TET: tetracyclin repressor; Avi: Avi tag; TEV: tobacco etch virus cleavage site; EGFP: enhanced green fluorescent protein; BirA: bifunctional protein biotin ligase BirA; IRES: internal ribosome entry site; HIS: poly-HIS purification tag; DELFIA: dissociation-enhanced lanthanide fluorescent immunoassay; 3-MBPP1: 1-(1,1-dimethylethyl)-3[(3-methylphenyl) methyl]-1H-pyrazolo[3,4-d] pyrimidin-4-amine; BSA: bovine serum albumin; ECL: Enhanced chemiluminescence
DOI: 10.6084/m9.figshare.17712194.v1
title: Uridine relieves MSCs and chondrocyte senescence <i>in vitvo</i> and exhibits the potential to treat osteoarthritis <i>in vivo</i>

description: Osteoarthritis (OA) is a degenerative disease of extremely high incidence in the elderly. Therefore, anti-aging may be an important prerequisite for treating OA. The senescence of chondrocytes and mesenchymal stem cells (MSCs) is one of the important factors that causes OA. Here, the effect of uridine (which is a functional food derived from plants or animals) on senescence of chondrocytes and MSCs was evaluated in <i>in vivo</i> and <i>in vitro</i> experiments. For this, we established the senescence model of chondrocyte and MSCs <i>in vitro</i>, and established the OA model <i>in vivo</i>, and a series of experiments (such as CLSM, ELISA, Western blot, etc.) were conducted to evaluate the effect of uridine on chondrocyte and MSCs senescence. The results showed that uridine could alleviate chondrocyte and MSCs senescence <i>in vitro</i> by evaluating a series of aging markers. Furthermore, uridine could also relieve OA <i>in vivo</i>. In summary, in the present work, we found that uridine can alleviate chondrocyte and MSCs senescence in <i>in vitro</i> and <i>in vivo</i> experiments. Uridine has shown great potential in the treatment of OA <i>in vivo</i>, suggesting that uridine could be used to treat and prevent OA induced by aging, and has potential clinical applications in future.
DOI: 10.6084/m9.figshare.17712194
title: Uridine relieves MSCs and chondrocyte senescence <i>in vitvo</i> and exhibits the potential to treat osteoarthritis <i>in vivo</i>

description: Osteoarthritis (OA) is a degenerative disease of extremely high incidence in the elderly. Therefore, anti-aging may be an important prerequisite for treating OA. The senescence of chondrocytes and mesenchymal stem cells (MSCs) is one of the important factors that causes OA. Here, the effect of uridine (which is a functional food derived from plants or animals) on senescence of chondrocytes and MSCs was evaluated in <i>in vivo</i> and <i>in vitro</i> experiments. For this, we established the senescence model of chondrocyte and MSCs <i>in vitro</i>, and established the OA model <i>in vivo</i>, and a series of experiments (such as CLSM, ELISA, Western blot, etc.) were conducted to evaluate the effect of uridine on chondrocyte and MSCs senescence. The results showed that uridine could alleviate chondrocyte and MSCs senescence <i>in vitro</i> by evaluating a series of aging markers. Furthermore, uridine could also relieve OA <i>in vivo</i>. In summary, in the present work, we found that uridine can alleviate chondrocyte and MSCs senescence in <i>in vitro</i> and <i>in vivo</i> experiments. Uridine has shown great potential in the treatment of OA <i>in vivo</i>, suggesting that uridine could be used to treat and prevent OA induced by aging, and has potential clinical applications in future.
DOI: 10.6084/m9.figshare.20624165
title: microRNA-206 prevents hepatocellular carcinoma growth and metastasis via down-regulating CREB5 and inhibiting the PI3K/AKT signaling pathway

description: Hepatocellular carcinoma (HCC) is one of the most common cancers and has continued to increase in incidence worldwide. Moreover, the involvement of microRNAs (miRs) has been reported in the development and progression of HCC. Here, we investigated the role of miR-206 in HCC growth and metastasis. HCC-related microarray datasets were harvested to screen differentially expressed miRNAs in HCC samples followed by prediction of downstream target genes. The dual-luciferase reporter assay verified the target-binding relationship between miR-206 and CREB5. The human HCC cell line MHCC97-H was cultured <i>in vitro</i> and transfected with miR-206 mimic/inhibitor or sh-/oe-CREB5 for analyzing MHCC97-H cell biological functions. The orthotopic xenograft model of HCC mice was constructed to observe the tumorigenic ability of HCC cells <i>in vivo</i>. Bioinformatics analysis found that miR-206 may be involved in HCC growth and metastasis by targeting CREB5 and regulating PI3K/AKT signaling pathway. <i>In vivo</i> animal experiments found that CREB5 was significantly overexpressed in mouse HCC tissues. In HCC cells, miR-206 can target down-regulate the expression of CREB5, thereby inhibiting the activation of PI3K/AKT signaling pathway. Furthermore, <i>in vitro</i> cell experiments confirmed that overexpression of miR-206 could inhibit the PI3K/AKT signaling pathway by down-regulating CREB5 expression, thereby inhibiting the proliferation, migration and invasion of HCC cells. In conclusion, our results revealed that miR-206 could down-regulate the expression of CREB5 and inhibit the activation of PI3K/AKT signaling pathway, thereby preventing HCC growth and metastasis. <b>Abbreviations:</b> HCC: hepatocellular carcinoma; HBV or HCV: hepatitis B or C virus; miRNAs: microRNAs; CREB: cAMP response element-binding protein; CRE: cAMP response elements
DOI: 10.6084/m9.figshare.20624165.v1
title: microRNA-206 prevents hepatocellular carcinoma growth and metastasis via down-regulating CREB5 and inhibiting the PI3K/AKT signaling pathway

description: Hepatocellular carcinoma (HCC) is one of the most common cancers and has continued to increase in incidence worldwide. Moreover, the involvement of microRNAs (miRs) has been reported in the development and progression of HCC. Here, we investigated the role of miR-206 in HCC growth and metastasis. HCC-related microarray datasets were harvested to screen differentially expressed miRNAs in HCC samples followed by prediction of downstream target genes. The dual-luciferase reporter assay verified the target-binding relationship between miR-206 and CREB5. The human HCC cell line MHCC97-H was cultured <i>in vitro</i> and transfected with miR-206 mimic/inhibitor or sh-/oe-CREB5 for analyzing MHCC97-H cell biological functions. The orthotopic xenograft model of HCC mice was constructed to observe the tumorigenic ability of HCC cells <i>in vivo</i>. Bioinformatics analysis found that miR-206 may be involved in HCC growth and metastasis by targeting CREB5 and regulating PI3K/AKT signaling pathway. <i>In vivo</i> animal experiments found that CREB5 was significantly overexpressed in mouse HCC tissues. In HCC cells, miR-206 can target down-regulate the expression of CREB5, thereby inhibiting the activation of PI3K/AKT signaling pathway. Furthermore, <i>in vitro</i> cell experiments confirmed that overexpression of miR-206 could inhibit the PI3K/AKT signaling pathway by down-regulating CREB5 expression, thereby inhibiting the proliferation, migration and invasion of HCC cells. In conclusion, our results revealed that miR-206 could down-regulate the expression of CREB5 and inhibit the activation of PI3K/AKT signaling pathway, thereby preventing HCC growth and metastasis. <b>Abbreviations:</b> HCC: hepatocellular carcinoma; HBV or HCV: hepatitis B or C virus; miRNAs: microRNAs; CREB: cAMP response element-binding protein; CRE: cAMP response elements
DOI: 10.6084/m9.figshare.19134163
title: STING agonist enhances the efficacy of programmed death-ligand 1 monoclonal antibody in breast cancer immunotherapy by activating the interferon-β signalling pathway

description: This study aimed to explore the role of a stimulator of interferon (IFN) gene (STING) agonist in breast cancer (BCa) immunotherapy. Clinical samples were collected from 37 patients with BCa. A tumor-bearing mouse model was established by injecting 4T1 cells into the mammary fat pad of mice. STING agonist and atezolizumab were injected in the mice twice a week for 2 weeks. Peripheral blood, tumor mass, lung, liver, brain cortex and kidney samples of the tumor-bearing mice were collected. Anti-IFN alpha receptor subunit 1 (IFNAR1) was used to treat 4T1 cells. Tumor tissues of patients with BCa exhibited lower STING and high programmed cell death protein 1 and programmed death-ligand 1 protein expressions. The STING agonist inhibited 4T1 cell growth in mice (<i>P</i> &lt; 0.001) and increased the IFN-β level and phosphorylation of STING, TBK1, IRF3 and STAT1 in tumor mass of tumor-bearing mice (<i>P</i> &lt; 0.001). It synergized with atezolizumab to inhibit 4T1 cell growth in mice and increased tumor necrosis factor-α, IFN-β, interleukin-10 and IFN-γ levels in the peripheral blood and tumor mass (<i>P</i> &lt; 0.01). It synergized with atezolizumab to increase CD8+ cytotoxic T cells and decrease FOXP3+ Treg cells in the tumor-bearing mouse model. The STING agonist was nontoxic to the lung, liver, brain cortex and kidney. Anti-IFNAR1 reversed the STING agonist promotion on TBK1, IRF3 and STAT1 phosphorylation in 4T1 cells (<i>P</i> &lt; 0.01). STING agonists enhance the efficacy of atezolizumab in BCa immunotherapy by activating the IFN-β signaling pathway.
DOI: 10.6084/m9.figshare.19134163.v1
title: STING agonist enhances the efficacy of programmed death-ligand 1 monoclonal antibody in breast cancer immunotherapy by activating the interferon-β signalling pathway

description: This study aimed to explore the role of a stimulator of interferon (IFN) gene (STING) agonist in breast cancer (BCa) immunotherapy. Clinical samples were collected from 37 patients with BCa. A tumor-bearing mouse model was established by injecting 4T1 cells into the mammary fat pad of mice. STING agonist and atezolizumab were injected in the mice twice a week for 2 weeks. Peripheral blood, tumor mass, lung, liver, brain cortex and kidney samples of the tumor-bearing mice were collected. Anti-IFN alpha receptor subunit 1 (IFNAR1) was used to treat 4T1 cells. Tumor tissues of patients with BCa exhibited lower STING and high programmed cell death protein 1 and programmed death-ligand 1 protein expressions. The STING agonist inhibited 4T1 cell growth in mice (<i>P</i> &lt; 0.001) and increased the IFN-β level and phosphorylation of STING, TBK1, IRF3 and STAT1 in tumor mass of tumor-bearing mice (<i>P</i> &lt; 0.001). It synergized with atezolizumab to inhibit 4T1 cell growth in mice and increased tumor necrosis factor-α, IFN-β, interleukin-10 and IFN-γ levels in the peripheral blood and tumor mass (<i>P</i> &lt; 0.01). It synergized with atezolizumab to increase CD8+ cytotoxic T cells and decrease FOXP3+ Treg cells in the tumor-bearing mouse model. The STING agonist was nontoxic to the lung, liver, brain cortex and kidney. Anti-IFNAR1 reversed the STING agonist promotion on TBK1, IRF3 and STAT1 phosphorylation in 4T1 cells (<i>P</i> &lt; 0.01). STING agonists enhance the efficacy of atezolizumab in BCa immunotherapy by activating the IFN-β signaling pathway.
DOI: 10.34740/kaggle/dsv/9091772
title: Balochi Language to English Translation Dataset
DOI: 10.15468/dl.nwhvn2
title: Occurrence Download

description: A dataset containing 0 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Geometry POLYGON ((-180 0, -40 0, -40 80, -180 80, -180 0))",
 "HasGeospatialIssue is false",
 "HasCoordinate is true",
 "OccurrenceStatus is Present",
 {
 "not" : {
 "BasisOfRecord" : [
 "is one of (Fossil, Living Specimen)"
 ]
 }
 },
 "ScientificName is Speyeria diana"
 ]
}

 The dataset includes 0 records from 0 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0045888-240626123714530/datasets/export for details.
DOI: 10.15468/dl.ts3ajb
title: Occurrence Download

description: A dataset containing 9240 species occurrences available in GBIF matching the query:
{
 "and" : [
 "OccurrenceStatus is Present",
 "TaxonKey is Monarda didyma L."
 ]
}

 The dataset includes 9240 records from 227 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0045889-240626123714530/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.uyqfds
title: Occurrence Download

description: A dataset containing 4838 species occurrences available in GBIF matching the query:
{
 "DatasetKey" : [
 "is A georeferenced database of the edaphic biota currently available for Argentina"
 ]
}

 The dataset includes 4838 records from 1 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0045890-240626123714530/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.3rbzcp
title: Occurrence Download

description: A dataset containing 125 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Geometry POLYGON((-11.14723 40.24421,25.14723 40.24421,25.14723 54.75579,-11.14723 54.75579,-11.14723 40.24421))",
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "OccurrenceStatus is Present",
 "TaxonKey is Andrena alutacea E.Stöckhert, 1942"
 ]
}

 The dataset includes 125 records from 14 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0045891-240626123714530/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.ausqa6
title: Occurrence Download

description: A dataset containing 227 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is Chile",
 "TaxonKey is Cyprinodontiformes"
 ]
}

 The dataset includes 227 records from 21 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0045893-240626123714530/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.r29jv6
title: Occurrence Download

description: A dataset containing 758949 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is Benin",
 "OccurrenceStatus is Present",
 "TaxonKey is Plantae"
 ]
}

 The dataset includes 758949 records from 245 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0045887-240626123714530/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.9uzx5f
title: Occurrence Download

description: A dataset containing 8662 species occurrences available in GBIF matching the query:
{
 "DatasetKey" : [
 "is Size Spectra of the edaphic fauna of Argiudol typical soils of the rolling Pampa region, Argentina"
 ]
}

 The dataset includes 8662 records from 1 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0045894-240626123714530/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.5066/p96l8gnf
title: Magnetic Survey Data in Glastonbury, Connecticut 2023

description: A ground-based magnetic survey was conducted in Glastonbury, Connecticut. Magnetic surveys are passive, non-contact, surface geophysical methods that measure the total ambient magnetic field. The magnetic survey utilized a Geometrics G-858 MagMapper with dual cesium vapor magnetometers and a GEM Systems Base Station. Sixteen survey profiles, totaling 7 linear kilometers in length, were carried out along Tyron Road, Old Maids Lane, Great Pond Road, Kettle Pond Drive, Taylor Town Road, Trout Brook Crossing, and Cemetery Lane near Dinosaur Park. Many survey lines were completed in areas containing high amounts of urban infrastructure, which adversely effects these data by producing magnetic fields that can obscure the magnetic field of underlying geology.

Below are two child items.
The first child item contains nine profiles carried out along Tyron Road, Old Maids Lane, Great Pond Road, Kettle Pond Drive, and Taylor Town Road that include diurnal corrections from a base station.
The second child item contains seven profiles carried out along Trout Brook Crossing, and Cemetery Lane near Dinosaur Park that include a constant magnetic field average correction instead of using a base station.
DOI: 10.15468/dl.d4vkfa
title: Occurrence Download

description: A dataset containing 2231 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Diaphorina citri Kuwayama, 1908"
 ]
}

 The dataset includes 2231 records from 22 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0045895-240626123714530/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.3xcdm5
title: Occurrence Download

description: A dataset containing 796903 species occurrences available in GBIF matching the query:
{
 "and" : [
 "OccurrenceStatus is Present",
 "TaxonKey is Cirsium vulgare (Savi) Ten."
 ]
}

 The dataset includes 796903 records from 3548 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0045892-240626123714530/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.