cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.19076194
title: The activity level of follicular helper T cells in the peripheral blood of osteosarcoma patients is associated with poor prognosis

description: Osteosarcoma (OS) is solid tumors with high malignancy and incidence starting in the bones. OS pathogenesis has been proved to be closely associated with immune imbalance, and follicular helper T cells (Tfh) significantly affect host humoral immune homeostasis. However, there are few reports on the effect of Tfh cell activation on the prognosis of OS patients. Hence, this investigation on the changes in the proportion of peripheral blood Tfh cells in OS patients, and the relationship between their activity level and OS prognosis. We collected peripheral blood from patients with OS, benign bone tumor (BT group) and healthy subjects (Healthy group), respectively. The number of CD4<sup>+</sup>CXCR5<sup>+</sup> Tfh cell in peripheral blood was measured by flow cytometry and correlation analysis between its activity and OS clinicopathological characteristics was carried out. The data showed that in comparison with the BT and Healthy groups, higher proportion and activation level of peripheral blood CD4<sup>+</sup>CXCR5<sup>+</sup> Tfh cells in CD4<sup>+</sup> T cells were found in the OS group. In OS patients, increases of the proportion and activity level of Tfh cells were associated with poorly differentiated OS and tumor metastasis. Additionally, Kaplan-Meier and Cox regression analysis showed a longer overall survival in patients with low proportion of peripheral blood CD4<sup>+</sup>CXCR5<sup>+</sup> Tfh cells in CD4<sup>+</sup> T cells, and their activation level may be a prognostic factor in OS patients. In conclusion, peripheral blood CD4<sup>+</sup>CXCR5<sup>+</sup> Tfh cell activation in OS patients was associated with a poor prognosis. This study provided ideas for improving the clinical treatment of OS patients.
DOI: 10.6084/m9.figshare.19076194.v1
title: The activity level of follicular helper T cells in the peripheral blood of osteosarcoma patients is associated with poor prognosis

description: Osteosarcoma (OS) is solid tumors with high malignancy and incidence starting in the bones. OS pathogenesis has been proved to be closely associated with immune imbalance, and follicular helper T cells (Tfh) significantly affect host humoral immune homeostasis. However, there are few reports on the effect of Tfh cell activation on the prognosis of OS patients. Hence, this investigation on the changes in the proportion of peripheral blood Tfh cells in OS patients, and the relationship between their activity level and OS prognosis. We collected peripheral blood from patients with OS, benign bone tumor (BT group) and healthy subjects (Healthy group), respectively. The number of CD4<sup>+</sup>CXCR5<sup>+</sup> Tfh cell in peripheral blood was measured by flow cytometry and correlation analysis between its activity and OS clinicopathological characteristics was carried out. The data showed that in comparison with the BT and Healthy groups, higher proportion and activation level of peripheral blood CD4<sup>+</sup>CXCR5<sup>+</sup> Tfh cells in CD4<sup>+</sup> T cells were found in the OS group. In OS patients, increases of the proportion and activity level of Tfh cells were associated with poorly differentiated OS and tumor metastasis. Additionally, Kaplan-Meier and Cox regression analysis showed a longer overall survival in patients with low proportion of peripheral blood CD4<sup>+</sup>CXCR5<sup>+</sup> Tfh cells in CD4<sup>+</sup> T cells, and their activation level may be a prognostic factor in OS patients. In conclusion, peripheral blood CD4<sup>+</sup>CXCR5<sup>+</sup> Tfh cell activation in OS patients was associated with a poor prognosis. This study provided ideas for improving the clinical treatment of OS patients.
DOI: 10.6084/m9.figshare.19121708
title: Depletion of mmu_circ_0001751 (circular RNA Carm1) protects against acute cerebral infarction injuries by binding with microRNA-3098-3p to regulate acyl-CoA synthetase long-chain family member 4

description: Circular RNAs (circRNAs) play a critical role in acute cerebral infarction (ACI). Our research discussed the effect of circ-Carm1 in ACI and its potential molecular mechanisms. Healthy controls and patients with ACI were included in this study. The establishment of an oxygen and glucose deprivation/reoxygenation (OGD/R) model of HT22 cells was conducted to mimic ACI <i>in vitro</i>. Quantitative reverse transcription polymerase chain reaction was conducted to determine mRNA levels extracted from serum and HT22 cell samples, and Western blotting was performed to determine protein levels. Terminal deoxynucleotidyl transferase dUTP nick end labeling and cell counting kit 8 assays were conducted to evaluate cellular functions. Concentrations of Fe<sup>2+</sup> and malondialdehyde, and levels of transferrin receptor 1, glutathione peroxidase 4, and glutathione were evaluated to determine ferroptosis in OGD/R-induced HT22 cells. The binding relationships between mRNAs and miRNAs were verified. circ-Carm1 was highly expressed in OGD/R-treated HT22 cells. Deficiency of circ-Carm1 restored cell viability and suppressed ferroptosis in OGD/R-induced HT22 cells. miR-3098-3p was predicted to be a target of circ-Carm1. The miR-3098-3p inhibitor partly neutralized the functions of circ-Carm1 in OGD/R-induced HT22 cells. Furthermore, acyl-CoA synthetase long-chain family member 4 (ACSL4) was confirmed to be a downstream target of miR-3098-3p and was elevated in OGD/R-induced HT22 cells. Overexpression of ACSL4 mitigated the functions of miR-3098-3p and accelerated HT22 cell dysfunction. Hence, circ-Carm1 is upregulated in ACI. circ-Carm1 suppression protects HT22 cells from dysfunction by inhibiting ferroptosis. Therefore, inducing circ-Carm1 deficiency may be a promising therapeutic method for ACI.
DOI: 10.6084/m9.figshare.19121708.v1
title: Depletion of mmu_circ_0001751 (circular RNA Carm1) protects against acute cerebral infarction injuries by binding with microRNA-3098-3p to regulate acyl-CoA synthetase long-chain family member 4

description: Circular RNAs (circRNAs) play a critical role in acute cerebral infarction (ACI). Our research discussed the effect of circ-Carm1 in ACI and its potential molecular mechanisms. Healthy controls and patients with ACI were included in this study. The establishment of an oxygen and glucose deprivation/reoxygenation (OGD/R) model of HT22 cells was conducted to mimic ACI <i>in vitro</i>. Quantitative reverse transcription polymerase chain reaction was conducted to determine mRNA levels extracted from serum and HT22 cell samples, and Western blotting was performed to determine protein levels. Terminal deoxynucleotidyl transferase dUTP nick end labeling and cell counting kit 8 assays were conducted to evaluate cellular functions. Concentrations of Fe<sup>2+</sup> and malondialdehyde, and levels of transferrin receptor 1, glutathione peroxidase 4, and glutathione were evaluated to determine ferroptosis in OGD/R-induced HT22 cells. The binding relationships between mRNAs and miRNAs were verified. circ-Carm1 was highly expressed in OGD/R-treated HT22 cells. Deficiency of circ-Carm1 restored cell viability and suppressed ferroptosis in OGD/R-induced HT22 cells. miR-3098-3p was predicted to be a target of circ-Carm1. The miR-3098-3p inhibitor partly neutralized the functions of circ-Carm1 in OGD/R-induced HT22 cells. Furthermore, acyl-CoA synthetase long-chain family member 4 (ACSL4) was confirmed to be a downstream target of miR-3098-3p and was elevated in OGD/R-induced HT22 cells. Overexpression of ACSL4 mitigated the functions of miR-3098-3p and accelerated HT22 cell dysfunction. Hence, circ-Carm1 is upregulated in ACI. circ-Carm1 suppression protects HT22 cells from dysfunction by inhibiting ferroptosis. Therefore, inducing circ-Carm1 deficiency may be a promising therapeutic method for ACI.
DOI: 10.6084/m9.figshare.19145341
title: miR-139-3p/Kinesin family member 18B axis suppresses malignant progression of gastric cancer

description: miR-139-3p exerts tumor-suppressing functions in various cancers. We analyzed and identified that miR-139-3p expression was notably low in gastric cancer (GC) via edgeR differential analysis based on The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction (qRT-PCR) assay. The binding relationship between Kinesin Family Member 18B (KIF18B) and miR-139-3p was predicted by bioinformatics databases, and verified through dual-luciferase assay. Western blot and qRT-PCR results also indicated that miR-139-3p restrained KIF18 expression at mRNA and protein levels. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing, transwell, flow cytometry assays were introduced to evaluate cell proliferation, migration, invasion, and cell cycle, respectively, where the results indicated that upregulating miR-139-3p inhibited proliferative, migratory, and invasive abilities of GC cells, while caused cell-cycle arrest. Moreover, the results of rescue experiments illustrated that miR-139-3p hampered the progression of GC cells by targeting and suppressing KIF18B. To sum up, we concluded that miR-139-3p suppressed GC progression by targeting KIF18B.
DOI: 10.6084/m9.figshare.18865951
title: Secreted phosphoprotein 1 as a potential prognostic and immunotherapy biomarker in multiple human cancers

description: Secreted phosphoprotein 1 (<i>SPP1</i>) is involved in immune regulation, cell survival, and tumor progression. Studies have demonstrated that <i>SPP1</i> plays an important role in certain individual tumors. However, the expression profile and oncogenic features of <i>SPP1</i> in diverse cancers are remaining unknown. Therefore, we performed a comprehensive analysis using The Cancer Genome Atlas (TCGA) database. Raw data of 33 cancer types were download from the University of California Santa Cruz (UCSC) Xena website. The expression of <i>SPP1</i> and its relationship with tumor prognosis, immune invasion, tumor microenvironment, and immunotherapy were analyzed using the R language. The function analysis was conducted using Gene Set Enrichment Analysis (GSEA). The oncogenic features of <i>SPP1</i> was validated by wound-healing assay and EdU staining assay. <i>SPP1</i> highly expressed in most cancers. The expression of <i>SPP1</i> was significant related to prognosis, tumor mutation burden (TMB), microsatellite instability (MSI), and immune checkpoint genes, suggested that <i>SPP1</i> plays an essential role in the tumor immune microenvironment and immune cell infiltration. The immune/stromal scores correlated positively with the <i>SPP1</i> expression, and the relationship was affected by tumor heterogeneity and immunotherapy. In addition, <i>SPP1</i> could predict the response of tumor immunotherapy. Functional analysis revealed the <i>SPP1</i>-associated terms and pathways. Finally, <i>SPP1</i> significantly elevated cell proliferation and migration in A549, Huh7, HT-29, A2780 tumor cell lines. In conclusion, this study indicated that <i>SPP1</i> involved in tumorigenesis, tumor progression, and regulated tumor immune microenvironment, revealing <i>SPP1</i> might be a potential target for evaluating prognosis and immunotherapy in multiple cancers.
DOI: 10.6084/m9.figshare.18865951.v1
title: Secreted phosphoprotein 1 as a potential prognostic and immunotherapy biomarker in multiple human cancers

description: Secreted phosphoprotein 1 (<i>SPP1</i>) is involved in immune regulation, cell survival, and tumor progression. Studies have demonstrated that <i>SPP1</i> plays an important role in certain individual tumors. However, the expression profile and oncogenic features of <i>SPP1</i> in diverse cancers are remaining unknown. Therefore, we performed a comprehensive analysis using The Cancer Genome Atlas (TCGA) database. Raw data of 33 cancer types were download from the University of California Santa Cruz (UCSC) Xena website. The expression of <i>SPP1</i> and its relationship with tumor prognosis, immune invasion, tumor microenvironment, and immunotherapy were analyzed using the R language. The function analysis was conducted using Gene Set Enrichment Analysis (GSEA). The oncogenic features of <i>SPP1</i> was validated by wound-healing assay and EdU staining assay. <i>SPP1</i> highly expressed in most cancers. The expression of <i>SPP1</i> was significant related to prognosis, tumor mutation burden (TMB), microsatellite instability (MSI), and immune checkpoint genes, suggested that <i>SPP1</i> plays an essential role in the tumor immune microenvironment and immune cell infiltration. The immune/stromal scores correlated positively with the <i>SPP1</i> expression, and the relationship was affected by tumor heterogeneity and immunotherapy. In addition, <i>SPP1</i> could predict the response of tumor immunotherapy. Functional analysis revealed the <i>SPP1</i>-associated terms and pathways. Finally, <i>SPP1</i> significantly elevated cell proliferation and migration in A549, Huh7, HT-29, A2780 tumor cell lines. In conclusion, this study indicated that <i>SPP1</i> involved in tumorigenesis, tumor progression, and regulated tumor immune microenvironment, revealing <i>SPP1</i> might be a potential target for evaluating prognosis and immunotherapy in multiple cancers.
DOI: 10.6084/m9.figshare.19145341.v1
title: miR-139-3p/Kinesin family member 18B axis suppresses malignant progression of gastric cancer

description: miR-139-3p exerts tumor-suppressing functions in various cancers. We analyzed and identified that miR-139-3p expression was notably low in gastric cancer (GC) via edgeR differential analysis based on The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction (qRT-PCR) assay. The binding relationship between Kinesin Family Member 18B (KIF18B) and miR-139-3p was predicted by bioinformatics databases, and verified through dual-luciferase assay. Western blot and qRT-PCR results also indicated that miR-139-3p restrained KIF18 expression at mRNA and protein levels. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing, transwell, flow cytometry assays were introduced to evaluate cell proliferation, migration, invasion, and cell cycle, respectively, where the results indicated that upregulating miR-139-3p inhibited proliferative, migratory, and invasive abilities of GC cells, while caused cell-cycle arrest. Moreover, the results of rescue experiments illustrated that miR-139-3p hampered the progression of GC cells by targeting and suppressing KIF18B. To sum up, we concluded that miR-139-3p suppressed GC progression by targeting KIF18B.
DOI: 10.6084/m9.figshare.19168715
title: Exosomes-derived miR-154-5p attenuates esophageal squamous cell carcinoma progression and angiogenesis by targeting kinesin family member 14

description: Exosomes participate in the progression and angiogenesis of esophageal squamous cell carcinoma (ESCC). This study aimed to explore the effect and mechanism of exosomes-derived miR-154-5p on the progression and angiogenesis of ESCC. The exosomes with the diameter of 40–270 nm were successfully isolated from ESCC cells by ultracentrifugation. They were then assessed by transmission electron microscope (TEM), nanoparticle tracking analysis (NTA), and Western blotting. Kinesin family member 14 (KIF14) was upregulated, while miR-154-5p was downregulated in ESCC as examined by Quantitative Real-time PCR (qRT-PCR). Exosomes-derived miR-154-5p from ESCC cells was found to attenuate the cellular migration, invasion, and angiogenesis of ESCC using Cell Counting Kit-8 (CCK-8), wound healing assay, transwell migration assay, and tumor formation assays. Moreover, KIF14 was proven to be a direct downstream target gene of miR-154-5p in ESCC cells using luciferase assay. In conclusion, our study identified that exosomes-derived miR-154-5p attenuates ESCC progression and angiogenesis by targeting KIF14 <i>in vitro</i>, which might provide a novel approach for the diagnosis and treatment of ESCC.
DOI: 10.6084/m9.figshare.19168715.v1
title: Exosomes-derived miR-154-5p attenuates esophageal squamous cell carcinoma progression and angiogenesis by targeting kinesin family member 14

description: Exosomes participate in the progression and angiogenesis of esophageal squamous cell carcinoma (ESCC). This study aimed to explore the effect and mechanism of exosomes-derived miR-154-5p on the progression and angiogenesis of ESCC. The exosomes with the diameter of 40–270 nm were successfully isolated from ESCC cells by ultracentrifugation. They were then assessed by transmission electron microscope (TEM), nanoparticle tracking analysis (NTA), and Western blotting. Kinesin family member 14 (KIF14) was upregulated, while miR-154-5p was downregulated in ESCC as examined by Quantitative Real-time PCR (qRT-PCR). Exosomes-derived miR-154-5p from ESCC cells was found to attenuate the cellular migration, invasion, and angiogenesis of ESCC using Cell Counting Kit-8 (CCK-8), wound healing assay, transwell migration assay, and tumor formation assays. Moreover, KIF14 was proven to be a direct downstream target gene of miR-154-5p in ESCC cells using luciferase assay. In conclusion, our study identified that exosomes-derived miR-154-5p attenuates ESCC progression and angiogenesis by targeting KIF14 <i>in vitro</i>, which might provide a novel approach for the diagnosis and treatment of ESCC.
DOI: 10.6084/m9.figshare.19153961
title: Long non-coding RNA DSCAM-AS1 promotes pancreatic cancer progression via regulating the miR-136-5p/PBX3 axis

description: LncRNA down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) plays an important role in tumor progression, but its function in pancreatic cancer is unknown. DSCAM-AS1 level was evaluated by <i>in situ</i> hybridization (ISH) assay and qRT-PCR. DSCAM-AS1 was knocked down in pancreatic cancer cells, and its impacts on cell proliferation, invasion, and migration were detected. The binding relationship among DSCAM-AS1, miR-136-5p, and pre-B-cell leukemia homeobox 3 (PBX3) was investigated by bioinformatic analysis and luciferase reporter assay. An <i>in vivo</i> animal model was constructed to determine the role of DSCAM-AS1 in tumor growth. Our results showed that DSCAM-AS1 was elevated in tumor tissues of pancreatic cancer patients and cell lines. DSCAM-AS1 knockdown efficiently inhibited PANC-1 cell proliferation, migration, and invasion and suppressed tumor growth. DSCAM-AS1 could promote PBX3 expression by sponging miR-136-5p, and its function in pancreatic cancer was partially mediated by the miR-136-5p/PBX3 axis. Overall, DSCAM-AS1 knockdown inhibits pancreatic cancer progression by modulating the miR-136-5p/PBX3 axis.
DOI: 10.6084/m9.figshare.19153961.v1
title: Long non-coding RNA DSCAM-AS1 promotes pancreatic cancer progression via regulating the miR-136-5p/PBX3 axis

description: LncRNA down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) plays an important role in tumor progression, but its function in pancreatic cancer is unknown. DSCAM-AS1 level was evaluated by <i>in situ</i> hybridization (ISH) assay and qRT-PCR. DSCAM-AS1 was knocked down in pancreatic cancer cells, and its impacts on cell proliferation, invasion, and migration were detected. The binding relationship among DSCAM-AS1, miR-136-5p, and pre-B-cell leukemia homeobox 3 (PBX3) was investigated by bioinformatic analysis and luciferase reporter assay. An <i>in vivo</i> animal model was constructed to determine the role of DSCAM-AS1 in tumor growth. Our results showed that DSCAM-AS1 was elevated in tumor tissues of pancreatic cancer patients and cell lines. DSCAM-AS1 knockdown efficiently inhibited PANC-1 cell proliferation, migration, and invasion and suppressed tumor growth. DSCAM-AS1 could promote PBX3 expression by sponging miR-136-5p, and its function in pancreatic cancer was partially mediated by the miR-136-5p/PBX3 axis. Overall, DSCAM-AS1 knockdown inhibits pancreatic cancer progression by modulating the miR-136-5p/PBX3 axis.
DOI: 10.6084/m9.figshare.18514996
title: Knockdown of ADORA2A antisense RNA 1 inhibits cell proliferation and enhances imatinib sensitivity in chronic myeloid leukemia

description: Long non-coding RNAs (LncRNAs) exert important regulatory roles in chronic myeloid leukemia (CML). In this study, we aimed to investigate the potential role and molecular mechanism of lncRNA ADORA2A antisense RNA 1 (ADORA2A-AS1) in CML. We found that the expression of ADORA2A-AS1 was upregulated in CML. Further, knockdown of ADORA2A-AS1 inhibited the proliferation, induced apoptosis, arrested cell cycle, and enhanced imatinib sensitivity in CML cells. Besides, ADORA2A-AS1 promoted the expression of transforming growth factor-beta receptor 1 (TGFBR1) and ATP binding cassette subfamily C member 2 (ABCC2) via sponging miR-665, thereby exerting a tumor-promoting activity. Collectively, our results confirmed the oncogenic effect of ADORA2A-AS1 in CML, indicating that ADORA2A-AS1 is a promosing therapeutic target for CML.
DOI: 10.6084/m9.figshare.18514996.v1
title: Knockdown of ADORA2A antisense RNA 1 inhibits cell proliferation and enhances imatinib sensitivity in chronic myeloid leukemia

description: Long non-coding RNAs (LncRNAs) exert important regulatory roles in chronic myeloid leukemia (CML). In this study, we aimed to investigate the potential role and molecular mechanism of lncRNA ADORA2A antisense RNA 1 (ADORA2A-AS1) in CML. We found that the expression of ADORA2A-AS1 was upregulated in CML. Further, knockdown of ADORA2A-AS1 inhibited the proliferation, induced apoptosis, arrested cell cycle, and enhanced imatinib sensitivity in CML cells. Besides, ADORA2A-AS1 promoted the expression of transforming growth factor-beta receptor 1 (TGFBR1) and ATP binding cassette subfamily C member 2 (ABCC2) via sponging miR-665, thereby exerting a tumor-promoting activity. Collectively, our results confirmed the oncogenic effect of ADORA2A-AS1 in CML, indicating that ADORA2A-AS1 is a promosing therapeutic target for CML.
DOI: 10.6084/m9.figshare.18599937
title: Eukaryotic translation initiation factor 3 subunit B could serve as a potential prognostic predictor for breast cancer

description: The EIF3 gene family is essential in controlling translation initiation during the cell cycle. The significance of the EIF3 subunits as prognostic markers and therapeutic targets in breast cancer is not yet clear. We analyzed the expression of EIF3 subunits in breast cancer on the GEPIA and Oncomine databases and compared their expression in breast cancer and normal tissues using BRCA data downloaded from TCGA. Then we performed clinical survival analysis on the Kaplan–Meier Plotter database and clinicopathologic analysis on the bc-genexMiner v4.1 database. And EIF3B was chosen for mutation analysis via the Cancer SEA online tool. Meanwhile, we performed the immunohistochemical assay, real-time RT-PCR, and Western blotting to analyze EIF3B expression levels in breast cancer. An EIF3B knockdown and a negative control cell line were conducted for MTT assay and cell cycle analysis to assess cell growth. Specifically, the results of TCGA and online databases demonstrated that upregulated EIF3B was associated with poorer overall and advanced tumor progression. We also confirmed that EIF3B was more highly expressed in breast cancer cells and tissues than normal and correlated with a worse outcome. And knockdown of EIF3B expression inhibited the cell cycle and proliferation. Furthermore, EIF3B was highly mutated in breast cancer. Collectively, our results suggested EIF3B as a potential prognostic marker and therapeutic target for breast cancer.