cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.12851483
title: Novel agent DMAMCL suppresses osteosarcoma growth and decreases the stemness of osteosarcoma stem cell

description: Osteosarcoma (OS) is the most common primary malignancy of bone that mostly affects children, adolescents, and young people. Despite advances have been made in multimodal therapy of OS, the long-term survival rate has reached a plateau, and the main obstacles are bad response to chemotherapy and gained chemoresistance. In this study, we tested the therapeutic effect of a newly reported drug, DMAMCL, on OS. Five human OS cell lines (143B, MNNG, MG63, Saos-2, U-2OS), and the mouse fibroblast cell line (NIH3T3) and human retinal epithelial cell (ARPE19) were used. The anti-tumor effect of DMAMCL was studied by MTS assay or IncuCyte-Zoom (<i>in vitro</i>), and Xenograft-mice-model (<i>in vivo</i>). Changes of cell cycle, apoptotic cells, caspase3/7 activities, and stemness after DMAMCL treatment were investigated. BAX siRNAs were used to knockdown the expression of BAX. Expressions of CyclinB1, CDC2, BCL-2 family, PARP, CD133, and Nanog were measured by Western Blotting. DMAMCL-induced dose-dependent OS cell death <i>in vitro</i>, and suppressed tumor growth and extended the survival of xenograft-bearing mice. DMAMCL-induced G2/M phase arrest <i>in vitro</i>, and apoptosis both <i>in vitro</i> and <i>in vivo</i>. Down-regulation of BAX expression attenuated the DMAMCL-induced OS cell death <i>in vitro</i>. We also found that DMAMCL inhibited the stemness in OS cells. These results indicated that DMAMCL possess therapeutic value in OS and may be a promising candidate for the new drug discovery for OS therapy.
DOI: 10.6084/m9.figshare.12851483.v1
title: Novel agent DMAMCL suppresses osteosarcoma growth and decreases the stemness of osteosarcoma stem cell

description: Osteosarcoma (OS) is the most common primary malignancy of bone that mostly affects children, adolescents, and young people. Despite advances have been made in multimodal therapy of OS, the long-term survival rate has reached a plateau, and the main obstacles are bad response to chemotherapy and gained chemoresistance. In this study, we tested the therapeutic effect of a newly reported drug, DMAMCL, on OS. Five human OS cell lines (143B, MNNG, MG63, Saos-2, U-2OS), and the mouse fibroblast cell line (NIH3T3) and human retinal epithelial cell (ARPE19) were used. The anti-tumor effect of DMAMCL was studied by MTS assay or IncuCyte-Zoom (<i>in vitro</i>), and Xenograft-mice-model (<i>in vivo</i>). Changes of cell cycle, apoptotic cells, caspase3/7 activities, and stemness after DMAMCL treatment were investigated. BAX siRNAs were used to knockdown the expression of BAX. Expressions of CyclinB1, CDC2, BCL-2 family, PARP, CD133, and Nanog were measured by Western Blotting. DMAMCL-induced dose-dependent OS cell death <i>in vitro</i>, and suppressed tumor growth and extended the survival of xenograft-bearing mice. DMAMCL-induced G2/M phase arrest <i>in vitro</i>, and apoptosis both <i>in vitro</i> and <i>in vivo</i>. Down-regulation of BAX expression attenuated the DMAMCL-induced OS cell death <i>in vitro</i>. We also found that DMAMCL inhibited the stemness in OS cells. These results indicated that DMAMCL possess therapeutic value in OS and may be a promising candidate for the new drug discovery for OS therapy.
DOI: 10.6084/m9.figshare.12851483.v2
title: Novel agent DMAMCL suppresses osteosarcoma growth and decreases the stemness of osteosarcoma stem cell

description: Osteosarcoma (OS) is the most common primary malignancy of bone that mostly affects children, adolescents, and young people. Despite advances have been made in multimodal therapy of OS, the long-term survival rate has reached a plateau, and the main obstacles are bad response to chemotherapy and gained chemoresistance. In this study, we tested the therapeutic effect of a newly reported drug, DMAMCL, on OS. Five human OS cell lines (143B, MNNG, MG63, Saos-2, U-2OS), and the mouse fibroblast cell line (NIH3T3) and human retinal epithelial cell (ARPE19) were used. The anti-tumor effect of DMAMCL was studied by MTS assay or IncuCyte-Zoom (<i>in vitro</i>), and Xenograft-mice-model (<i>in vivo</i>). Changes of cell cycle, apoptotic cells, caspase3/7 activities, and stemness after DMAMCL treatment were investigated. BAX siRNAs were used to knockdown the expression of BAX. Expressions of CyclinB1, CDC2, BCL-2 family, PARP, CD133, and Nanog were measured by Western Blotting. DMAMCL-induced dose-dependent OS cell death <i>in vitro</i>, and suppressed tumor growth and extended the survival of xenograft-bearing mice. DMAMCL-induced G2/M phase arrest <i>in vitro</i>, and apoptosis both <i>in vitro</i> and <i>in vivo</i>. Down-regulation of BAX expression attenuated the DMAMCL-induced OS cell death <i>in vitro</i>. We also found that DMAMCL inhibited the stemness in OS cells. These results indicated that DMAMCL possess therapeutic value in OS and may be a promising candidate for the new drug discovery for OS therapy.
DOI: 10.6084/m9.figshare.12851483.v3
title: Novel agent DMAMCL suppresses osteosarcoma growth and decreases the stemness of osteosarcoma stem cell

description: Osteosarcoma (OS) is the most common primary malignancy of bone that mostly affects children, adolescents, and young people. Despite advances have been made in multimodal therapy of OS, the long-term survival rate has reached a plateau, and the main obstacles are bad response to chemotherapy and gained chemoresistance. In this study, we tested the therapeutic effect of a newly reported drug, DMAMCL, on OS. Five human OS cell lines (143B, MNNG, MG63, Saos-2, U-2OS), and the mouse fibroblast cell line (NIH3T3) and human retinal epithelial cell (ARPE19) were used. The anti-tumor effect of DMAMCL was studied by MTS assay or IncuCyte-Zoom (<i>in vitro</i>), and Xenograft-mice-model (<i>in vivo</i>). Changes of cell cycle, apoptotic cells, caspase3/7 activities, and stemness after DMAMCL treatment were investigated. BAX siRNAs were used to knockdown the expression of BAX. Expressions of CyclinB1, CDC2, BCL-2 family, PARP, CD133, and Nanog were measured by Western Blotting. DMAMCL-induced dose-dependent OS cell death <i>in vitro</i>, and suppressed tumor growth and extended the survival of xenograft-bearing mice. DMAMCL-induced G2/M phase arrest <i>in vitro</i>, and apoptosis both <i>in vitro</i> and <i>in vivo</i>. Down-regulation of BAX expression attenuated the DMAMCL-induced OS cell death <i>in vitro</i>. We also found that DMAMCL inhibited the stemness in OS cells. These results indicated that DMAMCL possess therapeutic value in OS and may be a promising candidate for the new drug discovery for OS therapy.
DOI: 10.6084/m9.figshare.7608605
title: Additional file 2: of A dynamic degradome landscape on miRNAs and their predicted targets in sugarcane caused by Sporisorium scitamineum stress

description: Table S3. List of 309 predicted target mRNAs and their function annotations. (XLSX 55 kb)
DOI: 10.6084/m9.figshare.7608605.v1
title: Additional file 2: of A dynamic degradome landscape on miRNAs and their predicted targets in sugarcane caused by Sporisorium scitamineum stress

description: Table S3. List of 309 predicted target mRNAs and their function annotations. (XLSX 55 kb)
DOI: 10.6084/m9.figshare.7608608
title: Additional file 4: of Proteomic analysis reveals response of differential wheat (Triticum aestivum L.) genotypes to oxygen deficiency stress

description: Table S2. Clustering of the DEPs using K-mean method (XLS 593 kb)
DOI: 10.6084/m9.figshare.7608608.v1
title: Additional file 4: of Proteomic analysis reveals response of differential wheat (Triticum aestivum L.) genotypes to oxygen deficiency stress

description: Table S2. Clustering of the DEPs using K-mean method (XLS 593 kb)
DOI: 10.6084/m9.figshare.7608614
title: Additional file 5: of Proteomic analysis reveals response of differential wheat (Triticum aestivum L.) genotypes to oxygen deficiency stress

description: Table S3. All identified proteins in this study (XLS 8212 kb)
DOI: 10.6084/m9.figshare.7608614.v1
title: Additional file 5: of Proteomic analysis reveals response of differential wheat (Triticum aestivum L.) genotypes to oxygen deficiency stress

description: Table S3. All identified proteins in this study (XLS 8212 kb)
DOI: 10.6084/m9.figshare.12851495
title: Long non-coding RNA SLC16A1-AS1: its multiple tumorigenesis features and regulatory role in cell cycle in oral squamous cell carcinoma

description: Altered expressions of long non-coding RNAs (lncRNAs) are potential cancer prognostic biomarkers that play a critical role in the development of tumorigenesis and metastasis of cancer. However, the relationship between the expression of lncRNAs in oral squamous cell carcinoma (OSCC) and the diagnosis, progression, and prognosis of OSCC has not been thoroughly elucidated. To identify the differentially expressed lncRNAs between OSCC tissue and normal tissue, RNA-Seq data were used. lncRNA SLC16A1-AS1 was significantly highly expressed in OSCC samples than that in normal samples. Systematic bioinformatics analysis revealed that SLC16A1-AS1 was associated with histological tumor grades and overall survival status, as well as copy number variation, somatic mutation, tumor mutation burden, tumor stemness, tumor microenvironment and infiltrating immune cells. According to three advanced bioinformatic algorithms prediction (WGCNA, GSEA and GSVA), SLC16A1-AS1 played an essential role in OSCC proliferation and its biological function was related to cell-cycle regulation. Loss-of-function experiments were performed to determine the biological functions of SLC16A1-AS in OSCC cells. Silencing SLC16A1-AS1 significantly reduced the cell proliferation rate and colony-forming ability in both CAL27 and SCC25 cell lines. Flow cytometry and western blot analysis revealed that SLC16A1-AS1 silencing induced G0/G1 cell cycle arrest and inhibited the expression of cyclin D1 in both CAL27 and SCC25 cells. In conclusion, our study comprehensively investigated the role of the lncRNA SLC16A1-AS1 in OSCC growth and proved that it may serve as a new diagnostic indicator and a new target for the treatment of OSCC.
DOI: 10.6084/m9.figshare.12851495.v1
title: Long non-coding RNA SLC16A1-AS1: its multiple tumorigenesis features and regulatory role in cell cycle in oral squamous cell carcinoma

description: Altered expressions of long non-coding RNAs (lncRNAs) are potential cancer prognostic biomarkers that play a critical role in the development of tumorigenesis and metastasis of cancer. However, the relationship between the expression of lncRNAs in oral squamous cell carcinoma (OSCC) and the diagnosis, progression, and prognosis of OSCC has not been thoroughly elucidated. To identify the differentially expressed lncRNAs between OSCC tissue and normal tissue, RNA-Seq data were used. lncRNA SLC16A1-AS1 was significantly highly expressed in OSCC samples than that in normal samples. Systematic bioinformatics analysis revealed that SLC16A1-AS1 was associated with histological tumor grades and overall survival status, as well as copy number variation, somatic mutation, tumor mutation burden, tumor stemness, tumor microenvironment and infiltrating immune cells. According to three advanced bioinformatic algorithms prediction (WGCNA, GSEA and GSVA), SLC16A1-AS1 played an essential role in OSCC proliferation and its biological function was related to cell-cycle regulation. Loss-of-function experiments were performed to determine the biological functions of SLC16A1-AS in OSCC cells. Silencing SLC16A1-AS1 significantly reduced the cell proliferation rate and colony-forming ability in both CAL27 and SCC25 cell lines. Flow cytometry and western blot analysis revealed that SLC16A1-AS1 silencing induced G0/G1 cell cycle arrest and inhibited the expression of cyclin D1 in both CAL27 and SCC25 cells. In conclusion, our study comprehensively investigated the role of the lncRNA SLC16A1-AS1 in OSCC growth and proved that it may serve as a new diagnostic indicator and a new target for the treatment of OSCC.
DOI: 10.6084/m9.figshare.12851495.v2
title: Long non-coding RNA SLC16A1-AS1: its multiple tumorigenesis features and regulatory role in cell cycle in oral squamous cell carcinoma

description: Altered expressions of long non-coding RNAs (lncRNAs) are potential cancer prognostic biomarkers that play a critical role in the development of tumorigenesis and metastasis of cancer. However, the relationship between the expression of lncRNAs in oral squamous cell carcinoma (OSCC) and the diagnosis, progression, and prognosis of OSCC has not been thoroughly elucidated. To identify the differentially expressed lncRNAs between OSCC tissue and normal tissue, RNA-Seq data were used. lncRNA SLC16A1-AS1 was significantly highly expressed in OSCC samples than that in normal samples. Systematic bioinformatics analysis revealed that SLC16A1-AS1 was associated with histological tumor grades and overall survival status, as well as copy number variation, somatic mutation, tumor mutation burden, tumor stemness, tumor microenvironment and infiltrating immune cells. According to three advanced bioinformatic algorithms prediction (WGCNA, GSEA and GSVA), SLC16A1-AS1 played an essential role in OSCC proliferation and its biological function was related to cell-cycle regulation. Loss-of-function experiments were performed to determine the biological functions of SLC16A1-AS in OSCC cells. Silencing SLC16A1-AS1 significantly reduced the cell proliferation rate and colony-forming ability in both CAL27 and SCC25 cell lines. Flow cytometry and western blot analysis revealed that SLC16A1-AS1 silencing induced G0/G1 cell cycle arrest and inhibited the expression of cyclin D1 in both CAL27 and SCC25 cells. In conclusion, our study comprehensively investigated the role of the lncRNA SLC16A1-AS1 in OSCC growth and proved that it may serve as a new diagnostic indicator and a new target for the treatment of OSCC.
DOI: 10.6084/m9.figshare.12851501
title: CircRNA-UBE2G1 regulates LPS-induced osteoarthritis through miR-373/HIF-1a axis

description: Osteoarthritis (OA) is a very common chronic and degenerative joint disease characterized by persistent destruction of articular cartilage. Recently, increasing evidence showed that circular RNAs (circRNAs) play critical roles in OA progression. However, the functions of circRNAs in OA and their underlying mechanisms of action remain unclear. In the present study, the expression levels of circRNA-UBE2G1 and HIF-1a were significantly increased in OA tissues, whereas miR‑373 expression was downregulated. Function assays showed that circRNA-UBE2G1 inhibition reduced the effects of LPS on C28/I2 cells viability and apoptosis. In terms of mechanism, we revealed that circRNA-UBE2G1 binds to miR‑373 as competing endogenous RNAs (ceRNAs). HIF-1a might act as a target of miR‑373. Moreover, miR‑373 suppression or HIF-1a overexpression restored the effects of circRNA-UBE2G1 downregulation on LPS-induced chondrocytes injury. Collectively, our data suggest that circRNA-UBE2G1 facilitates the progression in the LPS-induced OA cell model via regulating the miR‑373/HIF-1a axis. OA: Osteoarthritis; Circular RNAs; miRNAs: MicroRNAs; Mut: Mutant; WT: Wild type; UTR: Untranslated region.
DOI: 10.6084/m9.figshare.12851501.v2
title: CircRNA-UBE2G1 regulates LPS-induced osteoarthritis through miR-373/HIF-1a axis

description: Osteoarthritis (OA) is a very common chronic and degenerative joint disease characterized by persistent destruction of articular cartilage. Recently, increasing evidence showed that circular RNAs (circRNAs) play critical roles in OA progression. However, the functions of circRNAs in OA and their underlying mechanisms of action remain unclear. In the present study, the expression levels of circRNA-UBE2G1 and HIF-1a were significantly increased in OA tissues, whereas miR‑373 expression was downregulated. Function assays showed that circRNA-UBE2G1 inhibition reduced the effects of LPS on C28/I2 cells viability and apoptosis. In terms of mechanism, we revealed that circRNA-UBE2G1 binds to miR‑373 as competing endogenous RNAs (ceRNAs). HIF-1a might act as a target of miR‑373. Moreover, miR‑373 suppression or HIF-1a overexpression restored the effects of circRNA-UBE2G1 downregulation on LPS-induced chondrocytes injury. Collectively, our data suggest that circRNA-UBE2G1 facilitates the progression in the LPS-induced OA cell model via regulating the miR‑373/HIF-1a axis. OA: Osteoarthritis; Circular RNAs; miRNAs: MicroRNAs; Mut: Mutant; WT: Wild type; UTR: Untranslated region.
DOI: 10.6084/m9.figshare.12851501.v1
title: CircRNA-UBE2G1 regulates LPS-induced osteoarthritis through miR-373/HIF-1a axis

description: Osteoarthritis (OA) is a very common chronic and degenerative joint disease characterized by persistent destruction of articular cartilage. Recently, increasing evidence showed that circular RNAs (circRNAs) play critical roles in OA progression. However, the functions of circRNAs in OA and their underlying mechanisms of action remain unclear. In the present study, the expression levels of circRNA-UBE2G1 and HIF-1a were significantly increased in OA tissues, whereas miR‑373 expression was downregulated. Function assays showed that circRNA-UBE2G1 inhibition reduced the effects of LPS on C28/I2 cells viability and apoptosis. In terms of mechanism, we revealed that circRNA-UBE2G1 binds to miR‑373 as competing endogenous RNAs (ceRNAs). HIF-1a might act as a target of miR‑373. Moreover, miR‑373 suppression or HIF-1a overexpression restored the effects of circRNA-UBE2G1 downregulation on LPS-induced chondrocytes injury. Collectively, our data suggest that circRNA-UBE2G1 facilitates the progression in the LPS-induced OA cell model via regulating the miR‑373/HIF-1a axis. OA: Osteoarthritis; Circular RNAs; miRNAs: MicroRNAs; Mut: Mutant; WT: Wild type; UTR: Untranslated region.
DOI: 10.6084/m9.figshare.7608629
title: Additional file 10: of Comparative analysis reveals the Genomic Islands in Pasteurella multocida population genetics: on Symbiosis and adaptability

description: Table S7. Predicted phage basic information. (XLSX 79 kb)
DOI: 10.6084/m9.figshare.7608629.v1
title: Additional file 10: of Comparative analysis reveals the Genomic Islands in Pasteurella multocida population genetics: on Symbiosis and adaptability

description: Table S7. Predicted phage basic information. (XLSX 79 kb)
DOI: 10.6084/m9.figshare.7608638
title: Additional file 11: of Comparative analysis reveals the Genomic Islands in Pasteurella multocida population genetics: on Symbiosis and adaptability

description: Table S6. Enriched genes of GIs in the accessory gene. (XLS 1835 kb)
DOI: 10.6084/m9.figshare.7608638.v1
title: Additional file 11: of Comparative analysis reveals the Genomic Islands in Pasteurella multocida population genetics: on Symbiosis and adaptability

description: Table S6. Enriched genes of GIs in the accessory gene. (XLS 1835 kb)
DOI: 10.6084/m9.figshare.12851522.v1
title: BMI1 promotes steroidogenesis through maintaining redox homeostasis in mouse MLTC-1 and primary Leydig cells

description: In males, aging is accompanied by decline in serum testosterone levels due to impairment of testicular Leydig cells. The polycomb protein BMI1 has recently been identified as an anti-aging factor. In our previous study, BMI1 null mice showed decreased serum testosterone and Leydig cell population, excessive oxidative stress and p16/p19 signaling activation. However, a cause-and-effect relationship between phenotypes and pathways was not investigated. Here, we used the rescue approach to study the role of oxidative stress or p16/p19 in BMI1-mediated steroidogenesis. Our results revealed that treatment with antioxidant NAC, but not down-regulation of p16/p19, largely rescued cell senescence, DNA damage and steroidogenesis in BMI1-deficient mouse MLTC-1 and primary Leydig cells. Collectively, our study demonstrates that BMI1 orchestrates steroidogenesis mainly through maintaining redox homeostasis, and thus, BMI1 may be a novel and potential therapeutic target for treatment of hypogonadism.
DOI: 10.6084/m9.figshare.12851528.v1
title: Hsa-miR-425-5p promotes tumor growth and metastasis by activating the CTNND1-mediated β-catenin pathway and EMT in colorectal cancer

description: Colorectal cancer (CRC) is a common malignancy with high mortality. However, the roles of miR-425-5p and its underlying mechanism in CRC remain unknown. Here, RT-qPCR confirmed that miR-425-5p expression was increased by miR-425-5p mimic in SW480 cells and decreased by miR-425-5p inhibitor in LOVO cells. CCK-8, flow cytometry, wound healing and transwell assays revealed that the increased miR-425-5p promoted cell viability, cell cycle entry, migration and invasion in CRC. Besides, miR-425-5p overexpression induced epithelial–mesenchymal transition (EMT) with upregulation of Fibronectin, N-cadherin, Vimentin, and downregulation of E-cadherin. Moreover, miR-425-5p overexpression induced c-myc, Cyclin D1 and MMP7 levels, and promoted β-catenin translocation to the nucleus. Knockdown of miR-425-5p exerted opposite effects. Luciferase reporter assay indicated that miR-425-5p directly targeted CTNND1. Overexpression of miR-425-5p repressed CTNND1 expression at mRNA and protein levels. Silencing of CTNND1 had the inhibitory effect of miR-425-5p inhibitor on cell proliferation, migration, invasion, EMT, and the activation of β-catenin signaling pathway. Furthermore, miR-425-5p promoted tumor growth and metastasis in vivo. In conclusion, miR-425-5p may promote tumorigenesis and metastasis through activating CTNND1-mediated β-catenin pathway, which may provide therapeutic targets for human CRC.
DOI: 10.6084/m9.figshare.12851528.v2
title: Hsa-miR-425-5p promotes tumor growth and metastasis by activating the CTNND1-mediated β-catenin pathway and EMT in colorectal cancer

description: Colorectal cancer (CRC) is a common malignancy with high mortality. However, the roles of miR-425-5p and its underlying mechanism in CRC remain unknown. Here, RT-qPCR confirmed that miR-425-5p expression was increased by miR-425-5p mimic in SW480 cells and decreased by miR-425-5p inhibitor in LOVO cells. CCK-8, flow cytometry, wound healing and transwell assays revealed that the increased miR-425-5p promoted cell viability, cell cycle entry, migration and invasion in CRC. Besides, miR-425-5p overexpression induced epithelial–mesenchymal transition (EMT) with upregulation of Fibronectin, N-cadherin, Vimentin, and downregulation of E-cadherin. Moreover, miR-425-5p overexpression induced c-myc, Cyclin D1 and MMP7 levels, and promoted β-catenin translocation to the nucleus. Knockdown of miR-425-5p exerted opposite effects. Luciferase reporter assay indicated that miR-425-5p directly targeted CTNND1. Overexpression of miR-425-5p repressed CTNND1 expression at mRNA and protein levels. Silencing of CTNND1 had the inhibitory effect of miR-425-5p inhibitor on cell proliferation, migration, invasion, EMT, and the activation of β-catenin signaling pathway. Furthermore, miR-425-5p promoted tumor growth and metastasis in vivo. In conclusion, miR-425-5p may promote tumorigenesis and metastasis through activating CTNND1-mediated β-catenin pathway, which may provide therapeutic targets for human CRC.
DOI: 10.6084/m9.figshare.18094410
title: Additional file 1 of Identification of the molecular subgroups in asthma by gene expression profiles: airway inflammation implications

description: Additional file 1: Table S1. The definition of immune terms used for ssGSEA.
DOI: 10.6084/m9.figshare.18094410.v1
title: Additional file 1 of Identification of the molecular subgroups in asthma by gene expression profiles: airway inflammation implications

description: Additional file 1: Table S1. The definition of immune terms used for ssGSEA.
DOI: 10.6084/m9.figshare.18094413
title: Additional file 2 of Identification of the molecular subgroups in asthma by gene expression profiles: airway inflammation implications

description: Additional file 2: Table S2. The details of the genes in each of the WGCNA modules.