cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.13169436.v1
title: Prognostic and clinical significance of long non-coding RNA SNHG12 expression in various cancers

description: Recently, increasing studies suggested that lncRNA SNHG12 was aberrantly expressed in kinds of cancers. However, definite prognostic value of SNHG12 remains unclear. We conducted this meta-analysis to evaluate the association between SNHG12 expression level and cancer prognosis. A literature retrieval was conducted by searching kinds of databases. The meta-analysis was performed by using Revman 5.2 and Stata 12.0 software. Besides, The Cancer Genome Atlas dataset was analyzed to validate the results in our meta-analysis via using Gene Expression Profiling Interactive Analysis. The pooled results showed that high SNHG12 expression significantly indicated worse overall survival and recurrence-free survival. Tumor type, sample size, survival analysis method, and cutoff value did not alter SNHG12 prognosis value according to stratified analysis results. Additionally, higher expression of SNHG12 suggested unfavorable clinicopathological outcomes including larger tumor size, lymph node metastasis, distant metastasis, and advanced clinical stage. Online cross-validation in TCGA dataset further indicated that cancer patients with upregulated SNHG12 expression had worse overall survival and disease-free survival. Therefore, elevated SNHG12 expression was associated with poor survival and unfavorable clinical outcomes in various cancers, and therefore might be a potential prognostic biomarker in human cancers. <b>Abbreviations</b> Akt: protein kinase B; CESC: cervical squamous cell carcinoma and endocervical adenocarcinoma; ceRNA: competitive endogenous RNA; CNKI: China National Knowledge Infrastructure; CI: confidence interval; CCNE1: cyclin E1; COAD: colon adenocarcinoma; DM: distant metastasis; DFS: disease-free survival; EMT: epithelial–mesenchymal transition; FISH: fluorescence in situ hybridization; FIGO: the International Federation of Gynecology and Obstetrics; GEPIA: Gene Expression Profiling Interactive Analysis; HR: hazard ratio; HIFα: hypoxia-inducible factor 1 α; KIRC: kidney renal clear cell carcinoma; KIRP: kidney renal papillary cell carcinoma; LIHC: hepatocellular carcinoma; LNM: lymph node metastasis; mTOR: mechanistic target of rapamycin kinase; MMP-9: matrix metalloproteinase 9; MCL1: myeloid cell leukemia 1; MLK3: mixed-lineage protein kinase 3; N/A: not available; NOS: Newcastle-Ottawa Scale; OR: odd ratio; OS: overall survival; PSA: prostate-specific antigen; PI3K: phosphoinositide 3-kinase; qRT-PCR: quantitative real-time polymerase chain reaction; READ: rectum adenocarcinoma; RFS: recurrence-free survival; SARC: sarcoma; SNHG12: small nucleolar RNA host gene 12; STAT3: signal transducer and activator of transcription 3; SOX4: SRY-box transcription factor 4; SOX5: SRY-box transcription factor 5; STAD: stomach adenocarcinoma; TCGA: The Cancer Genome Atlas; TNM: tumor node metastasis; WWP1: WW domain-containing E3 ubiquitin protein ligase 1; WHO grade: World Health Organization grade; ZEB2: zinc finger E-box-binding homeobox 2
DOI: 10.6084/m9.figshare.11521905
title: Genome-wide analysis of <i>PYL-PP2C-SnRK2s</i> family in <i>Camellia sinensis</i>

description: Abscisic acid (ABA) signaling regulates plant growth and development and participates in response to abiotic stressors. However, details about the <i>PYL-PP2C-SnRK2</i> gene family, which is the core component of ABA signaling in <i>Camellia sinensis</i>, are unknown. In this work, we identified 14 pyrabactin resistance-likes (<i>PYLs</i>), 84 type 2C protein phosphatase (<i>PP2Cs</i>), and 8 SNF1-related protein kinase 2s (<i>SnRK2s</i>) from <i>C. sinensis</i>. The transcriptomic analysis indicated that <i>PYL-PP2C-SnRK2s</i> were associated with changes of leaf color and the response of <i>C. sinensis</i> to drought and salt stressors. Changes of the expression of <i>Snrk2s</i> were not significant in the process of leaf color change or drought and salt stress response, suggesting that <i>PYLs</i> and <i>PP2Cs</i> may not interact with <i>SnRK2s</i> in <i>C. sinensis</i> during these processes. Finally, Gene Regulatory Network (GRN) construction and interaction networks analysis demonstrated that <i>PYLs</i> and <i>PP2Cs</i> were associated with multiple metabolic pathways during the changes of leaf color.
DOI: 10.6084/m9.figshare.11521905.v2
title: Genome-wide analysis of <i>PYL-PP2C-SnRK2s</i> family in <i>Camellia sinensis</i>

description: Abscisic acid (ABA) signaling regulates plant growth and development and participates in response to abiotic stressors. However, details about the <i>PYL-PP2C-SnRK2</i> gene family, which is the core component of ABA signaling in <i>Camellia sinensis</i>, are unknown. In this work, we identified 14 pyrabactin resistance-likes (<i>PYLs</i>), 84 type 2C protein phosphatase (<i>PP2Cs</i>), and 8 SNF1-related protein kinase 2s (<i>SnRK2s</i>) from <i>C. sinensis</i>. The transcriptomic analysis indicated that <i>PYL-PP2C-SnRK2s</i> were associated with changes of leaf color and the response of <i>C. sinensis</i> to drought and salt stressors. Changes of the expression of <i>Snrk2s</i> were not significant in the process of leaf color change or drought and salt stress response, suggesting that <i>PYLs</i> and <i>PP2Cs</i> may not interact with <i>SnRK2s</i> in <i>C. sinensis</i> during these processes. Finally, Gene Regulatory Network (GRN) construction and interaction networks analysis demonstrated that <i>PYLs</i> and <i>PP2Cs</i> were associated with multiple metabolic pathways during the changes of leaf color.
DOI: 10.6084/m9.figshare.11988903
title: Improved production of recombinant <i>Rhizomucor miehei</i> lipase by coexpressing protein folding chaperones in <i>Pichia pastoris</i>, which triggered ER stress

description: <i>Rhizomucor miehei</i> lipase (RML) is a biocatalyst that widely used in laboratory and industrial. Previously, RML with a 70-amino acid propeptide (pRML) was cloned and expressed in <i>P. pastori</i><i>s</i>. Recombinant strains with (strain containing 4-copy <i>prml</i>) and without ER stress (strain containing 2-copy <i>prml</i>) were obtained. However, the effective expression of pRML in <i>P. pastoris</i> by coexpressing ER-related elements in pRML-produced strain with or without ER stress has not been reported to date. In this study, an efficient way to produce functional pRML was explored in <i>P. pastoris</i>. The coexpression of protein folding chaperones, including <i>PDI</i> and <i>ERO1</i>, in different strains with or without ER stress, was investigated. <i>PDI</i> overexpression only increased pRML production in 4-copy strain from 705 U/mL to 1430 U/mL because it alleviated the protein folded stress, increased the protein concentration from 0.56  mg/mL to 0.65 mg/mL, and improved enzyme-specific activity from 1238 U/mg to 2186 U/mg. However, <i>PDI</i> coexpression could not improve pRML production in the 2-copy strain because it increased protein folded stress, while <i>ERO1</i> coexpression in the two strains all had a negative effect on pRML expression. We also investigated the effect of the propeptide on the substrate specificity and the condition for pRML enzyme powder preparation. Results showed that the relative activity exceeded 80% when the substrates C8–C10 were detected at 35°C and pH 6, and C8–C12 at 45°C and pH 8. The optimal enzyme powder preparation pH was 7, and the maximum recovery rate for pRML was 73.19%.
DOI: 10.6084/m9.figshare.13133611
title: Systems pharmacology in combination with proteomics reveals underlying mechanisms of Xihuang pill against triple-negative breast cancer

description: Xihuang pill (XHP), a traditional Chinese herbal formula, has been clinically used as an adjuvant therapy against triple-negative breast cancer (TNBC) via inhibiting cancer cell invasion and proliferation, as well as promoting cancer cell apoptosis. However, its anti-TNBC bio-active ingredients and possible mechanisms are still unclear. Herein, the hub bio-active compounds and underlying mechanisms of XHP against TNBC were systematically elucidated by integrating systems pharmacology approach and <i>in vitro</i> proteomics analysis. Using systems pharmacology analysis and molecular docking evaluation, 28 bio-active compounds and 10 potential therapeutic targets of XHP were identified. Functional analysis showed that the core therapeutic targets against TNBC were mainly involved in epidermal growth factor receptor (EGFR)-phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathway to prevent cancer cell proliferation and angiogenesis, as well as to enhance cancer cell apoptosis. The <i>in vitro</i> proteomics analysis identified 153 differentially expressed proteins (DEPs), including HASP90AA1, AKT1, and EGFR, which were also identified as therapeutic targets against TNBC through systems pharmacology analysis. Protein function analysis showed that the DEPs were mainly involved in PI3K-AKT signaling pathway, which was consistent with the result of systems pharmacology, suggesting the reliability of systems pharmacology analysis. Taken together, these findings uncover the underlying mechanism of XHP against TNBC, and provide a scientific method for the rational development of traditional Chinese medicine.
DOI: 10.6084/m9.figshare.13133611.v1
title: Systems pharmacology in combination with proteomics reveals underlying mechanisms of Xihuang pill against triple-negative breast cancer

description: Xihuang pill (XHP), a traditional Chinese herbal formula, has been clinically used as an adjuvant therapy against triple-negative breast cancer (TNBC) via inhibiting cancer cell invasion and proliferation, as well as promoting cancer cell apoptosis. However, its anti-TNBC bio-active ingredients and possible mechanisms are still unclear. Herein, the hub bio-active compounds and underlying mechanisms of XHP against TNBC were systematically elucidated by integrating systems pharmacology approach and <i>in vitro</i> proteomics analysis. Using systems pharmacology analysis and molecular docking evaluation, 28 bio-active compounds and 10 potential therapeutic targets of XHP were identified. Functional analysis showed that the core therapeutic targets against TNBC were mainly involved in epidermal growth factor receptor (EGFR)-phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathway to prevent cancer cell proliferation and angiogenesis, as well as to enhance cancer cell apoptosis. The <i>in vitro</i> proteomics analysis identified 153 differentially expressed proteins (DEPs), including HASP90AA1, AKT1, and EGFR, which were also identified as therapeutic targets against TNBC through systems pharmacology analysis. Protein function analysis showed that the DEPs were mainly involved in PI3K-AKT signaling pathway, which was consistent with the result of systems pharmacology, suggesting the reliability of systems pharmacology analysis. Taken together, these findings uncover the underlying mechanism of XHP against TNBC, and provide a scientific method for the rational development of traditional Chinese medicine.
DOI: 10.6084/m9.figshare.11521905.v1
title: Genome-wide Analysis of <i>PYL-PP2C-SnRK2s</i> Family in <i>Camellia sinensis</i>

description: Abscisic acid (ABA) signaling regulates plant growth and development and participates in response to abiotic stressors. However, details about the <i>PYL-PP2C-SnRK2</i> gene family, which is the core component of ABA signaling in <i>Camellia sinensis</i>, are unknown. In this work, we identified 14 pyrabactin resistance-likes (<i>PYLs</i>), 84 type 2C protein phosphatase (<i>PP2Cs</i>), and 8 SNF1-related protein kinase 2s (<i>SnRK2s</i>) from <i>C. sinensis</i>. The transcriptomic analysis indicated that <i>PYL-PP2C-SnRK2s</i> are associated with changes of leaf color and the response of <i>C. sinensis</i> to drought and salt stressors. Changes of the expression of <i>Snrk2s</i> were not significant in the process of leaf color change or drought and salt stress response, suggesting that <i>PYLs</i> and <i>PP2Cs</i> may not interact with <i>Snrk2s</i> in <i>C. sinensis</i> during these processes. Finally, Gene Regulatory Network (GRN) construction and interaction networks analysis demonstrated that <i>PYLs</i> and <i>PP2Cs</i> were associated with multiple metabolic pathways during the changes of leaf color.
DOI: 10.6084/m9.figshare.13003600
title: Long intergenic noncoding RNA01134 accelerates hepatocellular carcinoma progression by sponging microRNA-4784 and downregulating structure specific recognition protein 1

description: Dysregulation of long noncoding RNAs (lncRNAs) has been suggested to foster the carcinogenesis of hepatocellular carcinoma (HCC). To date, the role of long intergenic noncoding RNA01134 (LINC01134) in HCC have never been researched yet. Herein, we found that LINC01134 was highly expressed in HCC tissues in comparison with the matched normal liver tissues and increased LINC01134 expression correlated with shorter overall survival of patients with HCC. Additionally, we demonstrated LINC01134 downregulation significantly suppressed the proliferation ability and colony formation capacity of HCC cells. Furthermore, we revealed that LINC01134 functioned as a competitive endogenous RNA (ceRNA) for miR-4784 to upregulate structure-specific recognition protein 1 (SSRP1) in HCC cells. Meanwhile, miR-4784 inhibitor or restoration of SSRP1 could markedly attenuate the inhibitory effect of LINC01134 downregulation on HCC cells. Taken together, LINC01134 may promote the carcinogenesis of HCC at least partly via the miR-4784/SSRP1 axis. Therefore, LINC01134/miR-4784/SSRP1 axis should be developed as the promising therapeutic target for HCC.
DOI: 10.6084/m9.figshare.13003600.v1
title: Long intergenic noncoding RNA01134 accelerates hepatocellular carcinoma progression by sponging microRNA-4784 and downregulating structure specific recognition protein 1

description: Dysregulation of long noncoding RNAs (lncRNAs) has been suggested to foster the carcinogenesis of hepatocellular carcinoma (HCC). To date, the role of long intergenic noncoding RNA01134 (LINC01134) in HCC have never been researched yet. Herein, we found that LINC01134 was highly expressed in HCC tissues in comparison with the matched normal liver tissues and increased LINC01134 expression correlated with shorter overall survival of patients with HCC. Additionally, we demonstrated LINC01134 downregulation significantly suppressed the proliferation ability and colony formation capacity of HCC cells. Furthermore, we revealed that LINC01134 functioned as a competitive endogenous RNA (ceRNA) for miR-4784 to upregulate structure-specific recognition protein 1 (SSRP1) in HCC cells. Meanwhile, miR-4784 inhibitor or restoration of SSRP1 could markedly attenuate the inhibitory effect of LINC01134 downregulation on HCC cells. Taken together, LINC01134 may promote the carcinogenesis of HCC at least partly via the miR-4784/SSRP1 axis. Therefore, LINC01134/miR-4784/SSRP1 axis should be developed as the promising therapeutic target for HCC.
DOI: 10.6084/m9.figshare.12851465
title: Histone-fold centromere protein W (CENP-W) is associated with the biological behavior of hepatocellular carcinoma cells

description: Centromere protein W (CENP-W), identified as a centromeric component, plays an important role in the cell life cycle. However, how <i>CENPW</i> expression affects biological processes in liver cancer cells remains unknown. In this article, we found that <i>CENPW</i> was overexpressed in liver cancer tissues. Low <i>CENPW</i> expression was correlated with a better prognosis in hepatocellular carcinoma (HCC) patients, compared to high <i>CENPW</i> expression. The results of qRT-PCR and western blot assay showed that <i>CENPW</i> was effectively knocked down in HCC cells using siRNA transfection. Cell proliferation, migration, and invasion were inhibited. Cell apoptosis rates were increased. The cells were arrested in the G2/M phase of the cell cycle. Subsequently, 127 differentially expressed genes (DEGs) were identified based on RNA-seq data. GO and KEGG enrichment and PPI network analysis were performed. The novel DEGs were found and mainly enriched in nucleosome assembly and the complement system. In summary, our study indicated that overexpression of <i>CENPW</i> implied unfavorable prognosis and <i>CENPW</i> might be the potential predictive biomarker in liver cancer. Downregulation of <i>CENPW</i> might inhibit the HCC developmentby regulating the expression of the molecules in nucleosomes and the complement system.
DOI: 10.6084/m9.figshare.12851465.v1
title: Histone-fold centromere protein W (CENP-W) is associated with the biological behavior of hepatocellular carcinoma cells

description: Centromere protein W (CENP-W), identified as a centromeric component, plays an important role in the cell life cycle. However, how <i>CENPW</i> expression affects biological processes in liver cancer cells remains unknown. In this article, we found that <i>CENPW</i> was overexpressed in liver cancer tissues. Low <i>CENPW</i> expression was correlated with a better prognosis in hepatocellular carcinoma (HCC) patients, compared to high <i>CENPW</i> expression. The results of qRT-PCR and western blot assay showed that <i>CENPW</i> was effectively knocked down in HCC cells using siRNA transfection. Cell proliferation, migration, and invasion were inhibited. Cell apoptosis rates were increased. The cells were arrested in the G2/M phase of the cell cycle. Subsequently, 127 differentially expressed genes (DEGs) were identified based on RNA-seq data. GO and KEGG enrichment and PPI network analysis were performed. The novel DEGs were found and mainly enriched in nucleosome assembly and the complement system. In summary, our study indicated that overexpression of <i>CENPW</i> implied unfavorable prognosis and <i>CENPW</i> might be the potential predictive biomarker in liver cancer. Downregulation of <i>CENPW</i> might inhibit the HCC developmentby regulating the expression of the molecules in nucleosomes and the complement system.
DOI: 10.6084/m9.figshare.13049345.v1
title: Mitochondrial serine protease Omi/HtrA2 accentuates brain ischemia/reperfusion injury in rats and oxidative stress injury in vitro by modulating mitochondrial stress proteins CHOP and ClpP and physically interacting with mitochondrial fusion protein OPA1

description: Serine protease Omi/HtrA2, a member of the HtrA family, is closely related to the maintenance of mitochondrial integrity and participates in apoptosis but its role in cerebral ischemia/reperfusion (I/R) injury and cellular oxidative stress response remains unclear. In this study, we found that I/R injury resulted in a time-dependent increase in Omi/HtrA2 expression in rat brain tissue. Inhibition of Omi/HtrA2 significantly inhibited XIAP cleavage in H<sub>2</sub>O<sub>2</sub>-induced PC12 cells. In addition, inhibition of Omi/HtrA2 significantly inhibited the up-regulation of mitochondrial stress proteins CHOP and ClpP, significantly reduced mitochondrial aggregation, and attenuated the decline of mitochondrial ΔΨm in PC12 cells. Studies show that there is a physical interaction between Omi/HtrA2 and OPA1. We found that Omi/HtrA2 and OPA1 are closely related to the oxidative stress mitochondrial response in PC12 cells. The current study has demonstrated that Omi/HtrA2 is upregulated in brain I/R injury <i>in vivo</i> and is implicated in mitochondrial response to oxidative stress <i>in vitro</i> by regulating mitochondrial stress proteins CHOP and CLpP and by interacting with mitochondrial cristae remodeling protein OPA1. These findings suggest that Omi/HtrA2 could be a candidate molecular target in diseases that involve oxidative stress such as in I/R injury. <b>Abbreviation</b>: ATP: Adenosine tripHospHate; Bax: BCL2-Associated X; Bcl-2: B-cell lympHoma-2; BSA: Albumin from bovine serum; DMEM: Dulbecco’s Minimum Essential Medium; DMSO: Dimethyl sulfoxide; HSP60: Heat shock protein60, 70; L-OPA1: Long forms of OPA1; Omi/HtrA2: high-temperature-regulated A2; MCAO: Middle cerebral artery occlusion; OPA1: Optic AtropHy; PBS: PHospHate buffered saline; PMSF: pHenylmethyl sulfonylfluoride; ROS: reactive oxygen species; SDS: Sodium dodecyl sulfate; S-OPA1: Short forms of OPA1; TTC: TripHenyltetrazalium chloride; XIAP: X-linked inhibitor apoptosis protein
DOI: 10.6084/m9.figshare.11829696
title: Development of a 15-gene signature for predicting prognosis in advanced colorectal cancer

description: Advanced colorectal cancer (CRC) is a significant cause of cancer mortality, with a poor prognosis. Here, we identified a novel prognostic signature for predicting survival of advanced CRC. Advanced CRC data were used (training set: n = 267 and validation set: n = 264). The survival analyses were investigated. The functional analysis of the prognostic signature was examined. In this study, our 15-gene signature was established and was an independent prognostic factor of advanced CRC. Stratification analyses also showed that this signature was still powerful for survival prediction in each stratum of age, gender, stage, and metastasis status. In mechanism, our signature involved in DNA replication, DNA damage, and cell cycle. Therefore, our findings suggested that this 15-gene signature has prognostic and predictive value in advanced CRC, which could be further used in personalized therapy for advanced CRC.
DOI: 10.6084/m9.figshare.11829696.v1
title: Development of a 15-gene signature for predicting prognosis in advanced colorectal cancer

description: Advanced colorectal cancer (CRC) is a significant cause of cancer mortality, with a poor prognosis. Here, we identified a novel prognostic signature for predicting survival of advanced CRC. Advanced CRC data were used (training set: n = 267 and validation set: n = 264). The survival analyses were investigated. The functional analysis of the prognostic signature was examined. In this study, our 15-gene signature was established and was an independent prognostic factor of advanced CRC. Stratification analyses also showed that this signature was still powerful for survival prediction in each stratum of age, gender, stage, and metastasis status. In mechanism, our signature involved in DNA replication, DNA damage, and cell cycle. Therefore, our findings suggested that this 15-gene signature has prognostic and predictive value in advanced CRC, which could be further used in personalized therapy for advanced CRC.
DOI: 10.6084/m9.figshare.12851474
title: ELFN1-AS1 accelerates cell proliferation, invasion and migration via regulating miR-497-3p/CLDN4 axis in ovarian cancer

description: Previous studies indicated that long non-coding RNAs (LncRNAs) were involved in the progression of multiple cancers including ovarian cancer (OV). LncRNA ELFN1-AS1 functioned as an oncogene in many cancers, but its potential roles in OV were largely unclear. In the current study, we were aimed at clarifying the biological roles and molecular mechanisms of ELFN1-AS1 in OV. We found that ELFN1-AS1 was significantly upregulated in OV tissues and cell lines. High expression of ELFN1-AS1 was associated with poor prognosis in OV patients. Knockdown of ELFN1-AS1 inhibited the proliferation, migration and invasion of SKOV3 cell lines and repressed tumor growth in xenografted ovarian models. Mechanistically, ELFN1-AS1 promoted the proliferation, migration and invasion of SKOV3 cells by sponging miR-497-3p. Additionally, CLDN4 was verified to be the target of miR-497-3p. Rescue experiments revealed that miR-497-3p inhibition could partly reverse the inhibitory effect of ELFN1-AS1 silencing on proliferation, migration and invasion of SKOV3 cell lines. Taken together, our findings indicated that ELFN1-AS1 acted as an oncogene in ovarian cancer through regulating the expression of CLDN4 by directly interacting with miR-497-3p. The results suggested that ELFN1-AS1 might act as a promising therapeutic target for OV.