cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.18599937.v1
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.
DOI: 10.6084/m9.figshare.19165917
title: LINC00467 facilitates the proliferation, migration and invasion of glioma via promoting the expression of inositol hexakisphosphate kinase 2 by binding to miR-339-3p

description: Our previous studies indicate that long noncoding RNA (lncRNA) LINC00467 can act as an oncogene to participate in the malignant progression of glioma, but the underlying molecular mechanism remains to be studied further. This study aimed to explore the biological role of the LINC00467/miR-339-3p/ inositol hexakisphosphate kinase 2 (IP6K2) regulatory axis in glioma. The Cancer Genome Atlas (TCGA), Oncomine databases and reverse transcription‑quantitative PCR (RT‑qPCR) were used to analyze IP6K2 expression in glioma. RT-PCR, EdU and transwell assays were conducted to observe the effect of IP6K2 on glioma cell proliferation, migration and invasion. Using bioinformatics analysis, RT-PCR, and dual luciferase reporter gene assay, the potential role of the LINC00467/miR-339-3p/IP6K2 regulatory axis in glioma was verified. The results showed that IP6K2 was up-regulated in glioma tissues and cell lines. Moreover, the expression level of IP6K2 was correlated with the clinical features of glioma patients. <i>In vitro</i> and <i>in vivo</i> experiments indicated that IP6K2 overexpression could promote the proliferation, migration, and invasion of glioma cells. Further bioinformatics analysis and <i>in vitro</i> assays revealed that LINC00467 could promote IP6K2 expression by binding to miR-339-3p and promote the malignant progression of glioma. Overall, LINC00467 could upregulate IP6K2 by binding to miR-339-3p and promote the proliferation, migration, and invasion of glioma cells. The LINC00467/miR-339-3p/IP6K2 regulatory axis might be a potential therapeutic target for glioma.
DOI: 10.6084/m9.figshare.19165917.v1
title: LINC00467 facilitates the proliferation, migration and invasion of glioma via promoting the expression of inositol hexakisphosphate kinase 2 by binding to miR-339-3p

description: Our previous studies indicate that long noncoding RNA (lncRNA) LINC00467 can act as an oncogene to participate in the malignant progression of glioma, but the underlying molecular mechanism remains to be studied further. This study aimed to explore the biological role of the LINC00467/miR-339-3p/ inositol hexakisphosphate kinase 2 (IP6K2) regulatory axis in glioma. The Cancer Genome Atlas (TCGA), Oncomine databases and reverse transcription‑quantitative PCR (RT‑qPCR) were used to analyze IP6K2 expression in glioma. RT-PCR, EdU and transwell assays were conducted to observe the effect of IP6K2 on glioma cell proliferation, migration and invasion. Using bioinformatics analysis, RT-PCR, and dual luciferase reporter gene assay, the potential role of the LINC00467/miR-339-3p/IP6K2 regulatory axis in glioma was verified. The results showed that IP6K2 was up-regulated in glioma tissues and cell lines. Moreover, the expression level of IP6K2 was correlated with the clinical features of glioma patients. <i>In vitro</i> and <i>in vivo</i> experiments indicated that IP6K2 overexpression could promote the proliferation, migration, and invasion of glioma cells. Further bioinformatics analysis and <i>in vitro</i> assays revealed that LINC00467 could promote IP6K2 expression by binding to miR-339-3p and promote the malignant progression of glioma. Overall, LINC00467 could upregulate IP6K2 by binding to miR-339-3p and promote the proliferation, migration, and invasion of glioma cells. The LINC00467/miR-339-3p/IP6K2 regulatory axis might be a potential therapeutic target for glioma.
DOI: 10.6084/m9.figshare.19165917.v2
title: LINC00467 facilitates the proliferation, migration and invasion of glioma via promoting the expression of inositol hexakisphosphate kinase 2 by binding to miR-339-3p

description: Our previous studies indicate that long noncoding RNA (lncRNA) LINC00467 can act as an oncogene to participate in the malignant progression of glioma, but the underlying molecular mechanism remains to be studied further. This study aimed to explore the biological role of the LINC00467/miR-339-3p/ inositol hexakisphosphate kinase 2 (IP6K2) regulatory axis in glioma. The Cancer Genome Atlas (TCGA), Oncomine databases and reverse transcription‑quantitative PCR (RT‑qPCR) were used to analyze IP6K2 expression in glioma. RT-PCR, EdU and transwell assays were conducted to observe the effect of IP6K2 on glioma cell proliferation, migration and invasion. Using bioinformatics analysis, RT-PCR, and dual luciferase reporter gene assay, the potential role of the LINC00467/miR-339-3p/IP6K2 regulatory axis in glioma was verified. The results showed that IP6K2 was up-regulated in glioma tissues and cell lines. Moreover, the expression level of IP6K2 was correlated with the clinical features of glioma patients. <i>In vitro</i> and <i>in vivo</i> experiments indicated that IP6K2 overexpression could promote the proliferation, migration, and invasion of glioma cells. Further bioinformatics analysis and <i>in vitro</i> assays revealed that LINC00467 could promote IP6K2 expression by binding to miR-339-3p and promote the malignant progression of glioma. Overall, LINC00467 could upregulate IP6K2 by binding to miR-339-3p and promote the proliferation, migration, and invasion of glioma cells. The LINC00467/miR-339-3p/IP6K2 regulatory axis might be a potential therapeutic target for glioma.
DOI: 10.6084/m9.figshare.18978382
title: Circular RNA hsa_circ_0006091 as a novel biomarker for hepatocellular carcinoma

description: Circular RNAs (circRNAs) are stable and extensively distributed non-coding RNA molecules that are differentially expressed in liver cancer tissues in the human body. In this study, we aimed to investigate circRNA as a novel candidate biomarker for hepatocellular carcinoma (HCC). For three groups of HCC and neighboring healthy tissues, the differentially expressed circRNAs were identified through high-throughput sequencing analysis. Reverse transcription PCR (RT-PCR) and quantitative polymerase chain reaction (qPCR) were employed for the evaluation of circRNAs that show an elevated expression level in HCC. The obtained results revealed the significantly differential expression of hsa_circ_0006091 in HCC. Then we obtained their target genes through biological analysis, followed by verifying the underlined target genes, and the regulator of G-protein signaling 12 (RGS12) showed an elevated expression level in HCC tissues. Finally, receiver operating characteristic (ROC) curve analysis was conducted on AFP, RGS12, and hsa_circ_0006091, and combined analysis was performed. Furthermore, hsa_circ_0006091 is a novel candidate biomarker for HCC and could improve the diagnostic strategies, prediction, and follow-up of HCC patients. The joint diagnosis of the hsa_circ_0006091&AFP and hsa_circ_0006091&RGS12 has diagnostic significance and can be used as a molecular marker for HCC diagnosis. <b>Abbreviations:</b> AUC:area under the ROC curve; ROC:Receptor Operating Characteristics; bp:base pair;mRNA:Messenger Ribonucleic acid;ceRNA:Competing endogenous RNA; RT-qPCR: Real time-quantitativen PCR technology; circRNA: circular RNA; HCC:Hepatocellular carcinoma;miRNA:microRNA;KEGG:Kyoto Encyclopedia of Genes and Genomes; RGS12:regulator of G-protein signaling 12; AFP:alpha fetoprotein; ncRNAs:non-coding RNAs; GEO:Gene Expression Omnibus; FDR:false discovery rate
DOI: 10.6084/m9.figshare.18978382.v1
title: Circular RNA hsa_circ_0006091 as a novel biomarker for hepatocellular carcinoma

description: Circular RNAs (circRNAs) are stable and extensively distributed non-coding RNA molecules that are differentially expressed in liver cancer tissues in the human body. In this study, we aimed to investigate circRNA as a novel candidate biomarker for hepatocellular carcinoma (HCC). For three groups of HCC and neighboring healthy tissues, the differentially expressed circRNAs were identified through high-throughput sequencing analysis. Reverse transcription PCR (RT-PCR) and quantitative polymerase chain reaction (qPCR) were employed for the evaluation of circRNAs that show an elevated expression level in HCC. The obtained results revealed the significantly differential expression of hsa_circ_0006091 in HCC. Then we obtained their target genes through biological analysis, followed by verifying the underlined target genes, and the regulator of G-protein signaling 12 (RGS12) showed an elevated expression level in HCC tissues. Finally, receiver operating characteristic (ROC) curve analysis was conducted on AFP, RGS12, and hsa_circ_0006091, and combined analysis was performed. Furthermore, hsa_circ_0006091 is a novel candidate biomarker for HCC and could improve the diagnostic strategies, prediction, and follow-up of HCC patients. The joint diagnosis of the hsa_circ_0006091&AFP and hsa_circ_0006091&RGS12 has diagnostic significance and can be used as a molecular marker for HCC diagnosis. <b>Abbreviations:</b> AUC:area under the ROC curve; ROC:Receptor Operating Characteristics; bp:base pair;mRNA:Messenger Ribonucleic acid;ceRNA:Competing endogenous RNA; RT-qPCR: Real time-quantitativen PCR technology; circRNA: circular RNA; HCC:Hepatocellular carcinoma;miRNA:microRNA;KEGG:Kyoto Encyclopedia of Genes and Genomes; RGS12:regulator of G-protein signaling 12; AFP:alpha fetoprotein; ncRNAs:non-coding RNAs; GEO:Gene Expression Omnibus; FDR:false discovery rate
DOI: 10.6084/m9.figshare.18462974.v1
title: Circular RNA hsa_circ_0032683 inhibits the progression of hepatocellular carcinoma by sponging microRNA-338-5p

description: Recently, several studies have been conducted on circRNA (circular RNA). circRNA regulates gene expression and plays a vital role in the occurrence and development of various tumors. However, the role and mechanism of hsa_circ_0032683 in hepatocellular carcinoma (HCC) is not studied yet. In GEO (Gene Expression Omnibus) database, hsa_circ_0032683 expression was significantly lower in HCC tissues than in normal liver tissues. In vitro and in vivo functional tests revealed that hsa_circ_0032683 could inhibit HCC cells proliferation and promote their apoptosis. Mechanically, hsa_circ_0032683 primarily exists in the cytoplasm and competes with microRNA-338-5p (miR-338-5p) to regulate reticulon 4(RTN4). Our experiments revealed that hsa_circ_0032683 receded the proliferation ability of HCC via ceRNA (competing endogenous RNAs) mechanism, which provided potential biomarkers and therapeutic targets for HCC patients. <b>Abbreviations:</b> circRNAs: circular RNA; HCC: hepatocellular carcinoma; RTN4: reticulon 4; ceRNA: competing endogenous RNA; GEO: Gene Expression Omnibus; miRNA: microRNA; CSCD: Cancer-specific circRNA database; CRI: Circular RNA Interactome; TCGA: The Cancer Genome Atlas; qRT‐PCR: quantitative real‐time PCR; NEK9:NIMA-related kinase nine; CSMD1: CUB and Sushi multiple domains 1; Tob1: transducer of ERBB2, 1; miR: microRNA; sh: short hairpin; WT: wild type; MUT: mutant
DOI: 10.6084/m9.figshare.18462974
title: Circular RNA hsa_circ_0032683 inhibits the progression of hepatocellular carcinoma by sponging microRNA-338-5p

description: Recently, several studies have been conducted on circRNA (circular RNA). circRNA regulates gene expression and plays a vital role in the occurrence and development of various tumors. However, the role and mechanism of hsa_circ_0032683 in hepatocellular carcinoma (HCC) is not studied yet. In GEO (Gene Expression Omnibus) database, hsa_circ_0032683 expression was significantly lower in HCC tissues than in normal liver tissues. In vitro and in vivo functional tests revealed that hsa_circ_0032683 could inhibit HCC cells proliferation and promote their apoptosis. Mechanically, hsa_circ_0032683 primarily exists in the cytoplasm and competes with microRNA-338-5p (miR-338-5p) to regulate reticulon 4(RTN4). Our experiments revealed that hsa_circ_0032683 receded the proliferation ability of HCC via ceRNA (competing endogenous RNAs) mechanism, which provided potential biomarkers and therapeutic targets for HCC patients. <b>Abbreviations:</b> circRNAs: circular RNA; HCC: hepatocellular carcinoma; RTN4: reticulon 4; ceRNA: competing endogenous RNA; GEO: Gene Expression Omnibus; miRNA: microRNA; CSCD: Cancer-specific circRNA database; CRI: Circular RNA Interactome; TCGA: The Cancer Genome Atlas; qRT‐PCR: quantitative real‐time PCR; NEK9:NIMA-related kinase nine; CSMD1: CUB and Sushi multiple domains 1; Tob1: transducer of ERBB2, 1; miR: microRNA; sh: short hairpin; WT: wild type; MUT: mutant
DOI: 10.6084/m9.figshare.18551244
title: Inflammatory activation and immune cell infiltration are main biological characteristics of SARS-CoV-2 infected myocardium

description: The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) can target cardiomyocytes (CMs) to directly invade the heart resulting in high mortality. This study aims to explore the biological characteristics of SARS-CoV-2 infected myocardium based on omics by collecting transcriptome data and analyzing them with a series of bioinformatics tools. Totally, 86 differentially expressed genes (DEGs) were discovered in SARS-CoV-2 infected CMs, and 15 miRNAs were discovered to target 60 genes. Functional enrichment analysis indicated that these DEGs were mainly enriched in the inflammatory signaling pathway. After the protein-protein interaction (PPI) network was constructed, several genes including CCL2 and CXCL8 were regarded as the hub genes. SRC inhibitor saracatinib was predicted to potentially act against the cardiac dysfunction induced by SARS-CoV-2. Among the 86 DEGs, 28 were validated to be dysregulated in SARS-CoV-2 infected hearts. Gene Set Enrichment Analysis (GSEA) analysis of Kyoto Encyclopedia of Genes and Genomes (KEGG) showed that malaria, IL-17 signaling pathway, and complement and coagulation cascades were significantly enriched. Immune infiltration analysis indicated that ‘naive B cells’ was significantly increased in the SARS-CoV-2 infected heart. The above results may help to improve the prognosis of patients with COVID-19.
DOI: 10.6084/m9.figshare.18551244.v1
title: Inflammatory activation and immune cell infiltration are main biological characteristics of SARS-CoV-2 infected myocardium

description: The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) can target cardiomyocytes (CMs) to directly invade the heart resulting in high mortality. This study aims to explore the biological characteristics of SARS-CoV-2 infected myocardium based on omics by collecting transcriptome data and analyzing them with a series of bioinformatics tools. Totally, 86 differentially expressed genes (DEGs) were discovered in SARS-CoV-2 infected CMs, and 15 miRNAs were discovered to target 60 genes. Functional enrichment analysis indicated that these DEGs were mainly enriched in the inflammatory signaling pathway. After the protein-protein interaction (PPI) network was constructed, several genes including CCL2 and CXCL8 were regarded as the hub genes. SRC inhibitor saracatinib was predicted to potentially act against the cardiac dysfunction induced by SARS-CoV-2. Among the 86 DEGs, 28 were validated to be dysregulated in SARS-CoV-2 infected hearts. Gene Set Enrichment Analysis (GSEA) analysis of Kyoto Encyclopedia of Genes and Genomes (KEGG) showed that malaria, IL-17 signaling pathway, and complement and coagulation cascades were significantly enriched. Immune infiltration analysis indicated that ‘naive B cells’ was significantly increased in the SARS-CoV-2 infected heart. The above results may help to improve the prognosis of patients with COVID-19.
DOI: 10.6084/m9.figshare.19115561
title: Foxhead box D1 promotes the partial epithelial-to-mesenchymal transition of laryngeal squamous cell carcinoma cells via transcriptionally activating the expression of zinc finger protein 532

description: The presence of cervical lymph node metastases has been considered as the most important adverse prognostic factor for patients with laryngeal squamous cell carcinoma (LSCC). However, the underlying mechanisms remain to be fully revealed. In this study, we explored the expression profile of <i>Foxhead box D1</i> (<i>FOXD1</i>), its association with epithelial-to-mesenchymal transition (EMT), and its downstream targets in LSCC. Bioinformatic analysis was performed based on the LSCC subset of The Cancer Genome Atlas-Head and Neck Squamous Cell Carcinoma (TCGA-HSNC) and Chromatin immunoprecipitation (ChIP)-seq data from Cistrome Data Browser. LSCC cell lines AMC-HN-8 and TU212 were used for <i>in vitro</i> studies. Results showed that <i>FOXD1</i> upregulation was associated with poor prognosis of LSCC. <i>FOXD1</i> knockdown reduced N-cadherin and Vimentin expression but increased E-cadherin expression in AMC-HN-8 cells. Its overexpression showed opposite effects in TU212 cells. FOXD1 could bind to the promoter of <i>ZNF532</i> and activate its transcription. <i>ZNF532</i> overexpression enhanced the invasion of both AMC-HN-8 and TU212 cells. In comparison, its knockdown significantly impaired their invasion. <i>ZNF532</i> knockdown nearly abrogated the alterations of EMT markers caused by <i>FOXD1</i> overexpression. Its overexpression largely rescued the phenotypes caused by <i>FOXD1</i> knockdown. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that <i>ZNF532</i> correlated genes are largely enriched in extracellular matrix regulations. LSCC patients with high <i>ZNF532</i> expression (top 50%) had a significantly worse progression-free survival. In summary, this study confirmed that FOXD1 promotes partial-EMT of LSCC cells via transcriptionally activating the expression of <i>ZNF532</i>.
DOI: 10.6084/m9.figshare.19115561.v1
title: Foxhead box D1 promotes the partial epithelial-to-mesenchymal transition of laryngeal squamous cell carcinoma cells via transcriptionally activating the expression of zinc finger protein 532

description: The presence of cervical lymph node metastases has been considered as the most important adverse prognostic factor for patients with laryngeal squamous cell carcinoma (LSCC). However, the underlying mechanisms remain to be fully revealed. In this study, we explored the expression profile of <i>Foxhead box D1</i> (<i>FOXD1</i>), its association with epithelial-to-mesenchymal transition (EMT), and its downstream targets in LSCC. Bioinformatic analysis was performed based on the LSCC subset of The Cancer Genome Atlas-Head and Neck Squamous Cell Carcinoma (TCGA-HSNC) and Chromatin immunoprecipitation (ChIP)-seq data from Cistrome Data Browser. LSCC cell lines AMC-HN-8 and TU212 were used for <i>in vitro</i> studies. Results showed that <i>FOXD1</i> upregulation was associated with poor prognosis of LSCC. <i>FOXD1</i> knockdown reduced N-cadherin and Vimentin expression but increased E-cadherin expression in AMC-HN-8 cells. Its overexpression showed opposite effects in TU212 cells. FOXD1 could bind to the promoter of <i>ZNF532</i> and activate its transcription. <i>ZNF532</i> overexpression enhanced the invasion of both AMC-HN-8 and TU212 cells. In comparison, its knockdown significantly impaired their invasion. <i>ZNF532</i> knockdown nearly abrogated the alterations of EMT markers caused by <i>FOXD1</i> overexpression. Its overexpression largely rescued the phenotypes caused by <i>FOXD1</i> knockdown. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that <i>ZNF532</i> correlated genes are largely enriched in extracellular matrix regulations. LSCC patients with high <i>ZNF532</i> expression (top 50%) had a significantly worse progression-free survival. In summary, this study confirmed that FOXD1 promotes partial-EMT of LSCC cells via transcriptionally activating the expression of <i>ZNF532</i>.
DOI: 10.6084/m9.figshare.19165809
title: Long non-coding RNA TRPM2 antisense RNA as a potential therapeutic target promotes tumorigenesis and metastasis in esophageal cancer

description: Esophageal cancer (EC) is one type of aggressive gastrointestinal cancers. The treatment of EC is challenging. Effective therapeutic targets require development. Long non-coding RNA TRPM2 antisense RNA (LncRNA TRPM2-AS) is considering a novel biomarker and therapeutic target for various types of cancer. However, the role of lncRNA TRPM2-AS in EC remains unknown. This study aimed to illustrate effects of LncRNA TRPM2-AS on EC growth and metastasis and potential underlying molecular mechanisms. LncRNA TRPM2-AS expression was determined in both EC tissues and cell lines by quantitative real-time polymerase-chain reaction (qRT-PCR). Cell proliferation ability was evaluated by cell counting kit-8 and colony formation assays. Cell apoptosis was analyzed by flow cytometry. Cell migration and invasion were determined using transwell. Epithelial–mesenchymal transition (EMT)-related markers expression were determined using qRT-PCR and Western blotting. Furthermore, potential lncRNA TRPM2-AS targeting miRNAs were predicted by public databases. The expression of five selected miRNAs were validated by qRT-PCR. We found that lncRNA TRPM2-AS expression was increased in EC tissues and cell lines compared with respective control. Silencing lncRNA TRPM2-AS suppressed EC cell proliferation, migration, and invasion while promoted cell apoptosis. Moreover, lncRNA TRPM2-AS knockdown reduced neural cadherin, vimentin, and matrix metallopeptidase 9 gene and protein expressions while increased epithelial cadherin expression. Furthermore, lncRNA TRPM2-AS knockdown promoted microRNA (miR)-1291, miR-6852-5p, and miR-138-5p expressions. Taken together, this study for the first time demonstrates that upregulation of lncRNA TRPM2-AS in EC promotes the growth and metastasis of EC likely through interacting with miR-1291, miR-6852-5p, and miR-138-5p.