cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1289845.v3
title: Frequent amplification of <i>PTP1B</i> is associated with poor survival of gastric cancer patients

description: The protein tyrosine phosphatase 1B (<i>PTP1B</i>), a non-transmembrane protein tyrosine phosphatase, has been implicated in gastric pathogenesis. Several lines of recent evidences have shown that <i>PTP1B</i> is highly amplified in breast and prostate cancers. The aim of this study was to investigate <i>PTP1B</i> amplification in gastric cancer and its association with poor prognosis of gastric cancer patients, and further determine the role of <i>PTP1B</i> in gastric tumorigenesis. Our data demonstrated that <i>PTP1B</i> was significantly up-regulated in gastric cancer tissues as compared with matched normal gastric tissues by using quantitative RT-PCR (qRT-PCR) assay. In addition, copy number analysis showed that <i>PTP1B</i> was amplified in 68/131 (51.9%) gastric cancer cases, whereas no amplification was found in the control subjects. Notably, <i>PTP1B</i> amplification was positively associated with its protein expression, and was significantly related to poor survival of gastric cancer patients. Knocking down <i>PTP1B</i> expression in gastric cancer cells significantly inhibited cell proliferation, colony formation, migration and invasion, and induced cell cycle arrested and apoptosis. Mechanically, <i>PTP1B</i> promotes gastric cancer cell proliferation, survival and invasiveness through modulating Src-related signaling pathways, such as Src/Ras/MAPK and Src/phosphatidylinositol-3-kinase (PI3K)/Akt pathways. Collectively, our data demonstrated frequent overexpression and amplification <i>PTP1B</i> in gastric cancer, and further determined the oncogenic role of <i>PTP1B</i> in gastric carcinogenesis. Importantly, <i>PTP1B</i> amplification predicts poor survival of gastric cancer patients.
DOI: 10.6084/m9.figshare.1289845.v5
title: Frequent amplification of <i>PTP1B</i> is associated with poor survival of gastric cancer patients

description: The protein tyrosine phosphatase 1B (<i>PTP1B</i>), a non-transmembrane protein tyrosine phosphatase, has been implicated in gastric pathogenesis. Several lines of recent evidences have shown that <i>PTP1B</i> is highly amplified in breast and prostate cancers. The aim of this study was to investigate <i>PTP1B</i> amplification in gastric cancer and its association with poor prognosis of gastric cancer patients, and further determine the role of <i>PTP1B</i> in gastric tumorigenesis. Our data demonstrated that <i>PTP1B</i> was significantly up-regulated in gastric cancer tissues as compared with matched normal gastric tissues by using quantitative RT-PCR (qRT-PCR) assay. In addition, copy number analysis showed that <i>PTP1B</i> was amplified in 68/131 (51.9%) gastric cancer cases, whereas no amplification was found in the control subjects. Notably, <i>PTP1B</i> amplification was positively associated with its protein expression, and was significantly related to poor survival of gastric cancer patients. Knocking down <i>PTP1B</i> expression in gastric cancer cells significantly inhibited cell proliferation, colony formation, migration and invasion, and induced cell cycle arrested and apoptosis. Mechanically, <i>PTP1B</i> promotes gastric cancer cell proliferation, survival and invasiveness through modulating Src-related signaling pathways, such as Src/Ras/MAPK and Src/phosphatidylinositol-3-kinase (PI3K)/Akt pathways. Collectively, our data demonstrated frequent overexpression and amplification <i>PTP1B</i> in gastric cancer, and further determined the oncogenic role of <i>PTP1B</i> in gastric carcinogenesis. Importantly, <i>PTP1B</i> amplification predicts poor survival of gastric cancer patients.
DOI: 10.6084/m9.figshare.1289845.v4
title: Frequent amplification of <i>PTP1B</i> is associated with poor survival of gastric cancer patients

description: The protein tyrosine phosphatase 1B (<i>PTP1B</i>), a non-transmembrane protein tyrosine phosphatase, has been implicated in gastric pathogenesis. Several lines of recent evidences have shown that <i>PTP1B</i> is highly amplified in breast and prostate cancers. The aim of this study was to investigate <i>PTP1B</i> amplification in gastric cancer and its association with poor prognosis of gastric cancer patients, and further determine the role of <i>PTP1B</i> in gastric tumorigenesis. Our data demonstrated that <i>PTP1B</i> was significantly up-regulated in gastric cancer tissues as compared with matched normal gastric tissues by using quantitative RT-PCR (qRT-PCR) assay. In addition, copy number analysis showed that <i>PTP1B</i> was amplified in 68/131 (51.9%) gastric cancer cases, whereas no amplification was found in the control subjects. Notably, <i>PTP1B</i> amplification was positively associated with its protein expression, and was significantly related to poor survival of gastric cancer patients. Knocking down <i>PTP1B</i> expression in gastric cancer cells significantly inhibited cell proliferation, colony formation, migration and invasion, and induced cell cycle arrested and apoptosis. Mechanically, <i>PTP1B</i> promotes gastric cancer cell proliferation, survival and invasiveness through modulating Src-related signaling pathways, such as Src/Ras/MAPK and Src/phosphatidylinositol-3-kinase (PI3K)/Akt pathways. Collectively, our data demonstrated frequent overexpression and amplification <i>PTP1B</i> in gastric cancer, and further determined the oncogenic role of <i>PTP1B</i> in gastric carcinogenesis. Importantly, <i>PTP1B</i> amplification predicts poor survival of gastric cancer patients.
DOI: 10.6084/m9.figshare.1290934
title: Origin of Triassic granites in central Hunan Province, South China: constraints from zircon U–Pb ages and Hf and O isotopes

description: Triassic granites crop out extensively in central Hunan Province, South China. Representative granites include the Baimashan, Weishan, and Ziyunshan plutons. Lithologically, these granites mainly comprise biotite monzogranite, two-mica granites, hornblende-biotite granite, hornblende-biotite monzogranite, and garnet-muscovite granite. These granites have <i>in situ</i> zircon secondary ion mass spectrum U–Pb ages between 223.2 ± 3.3 and 209.3 ± 4.0 Ma, indicating that they likely formed predominantly in the Late Triassic. These granitic plutons have similar zircon Hf and O isotopic compositions, with <i>ε</i><sub>Hf</sub>(<i>t</i>) values of −0.8 to −9.0, two-stage depleted mantle model ages (<i>T</i><sub>DM2</sub>) of 1.81–1.31 Ga, and weighted mean of <i>δ</i><sup>18</sup>O<sub>Zrc</sub> values of 8.53 ± 0.58‰ to 9.12 ± 0.28‰. Combined with U–Pb dating and Hf isotopic data, the elevated and variable <i>δ</i><sup>18</sup>O and <i>ε</i><sub>Hf</sub>(<i>t</i>) values of the individual granites indicate that these Triassic granites were likely produced by partial melting of upper Paleoproterozoic to lower Mesoproterozoic metasedimentary rocks and are S-type granites. The variable proportions of inherited zircons in certain samples with U–Pb ages of 627–992 Ma indicate the involvement of lower–middle Neoproterozoic crustal materials during magma crystallization through wall-rock contamination, which resulted in the wide range of isotopic compositions. Underplating of mantle-derived magma may have provided the thermal energy for partial melting of the upper Paleoproterozoic and lower Mesoproterozoic basements, thereby generating these late Triassic granites. The lack of positive <i>ε</i><sub>Hf</sub>(<i>t</i>) values and high <i>δ</i><sup>18</sup>O<sub>Zrc</sub> values indicate that the contribution of mantle-derived magmas to these granites may be insignificant.
DOI: 10.6084/m9.figshare.1290934.v2
title: Origin of Triassic granites in central Hunan Province, South China: constraints from zircon U–Pb ages and Hf and O isotopes

description: Triassic granites crop out extensively in central Hunan Province, South China. Representative granites include the Baimashan, Weishan, and Ziyunshan plutons. Lithologically, these granites mainly comprise biotite monzogranite, two-mica granites, hornblende-biotite granite, hornblende-biotite monzogranite, and garnet-muscovite granite. These granites have <i>in situ</i> zircon secondary ion mass spectrum U–Pb ages between 223.2 ± 3.3 and 209.3 ± 4.0 Ma, indicating that they likely formed predominantly in the Late Triassic. These granitic plutons have similar zircon Hf and O isotopic compositions, with <i>ε</i><sub>Hf</sub>(<i>t</i>) values of −0.8 to −9.0, two-stage depleted mantle model ages (<i>T</i><sub>DM2</sub>) of 1.81–1.31 Ga, and weighted mean of <i>δ</i><sup>18</sup>O<sub>Zrc</sub> values of 8.53 ± 0.58‰ to 9.12 ± 0.28‰. Combined with U–Pb dating and Hf isotopic data, the elevated and variable <i>δ</i><sup>18</sup>O and <i>ε</i><sub>Hf</sub>(<i>t</i>) values of the individual granites indicate that these Triassic granites were likely produced by partial melting of upper Paleoproterozoic to lower Mesoproterozoic metasedimentary rocks and are S-type granites. The variable proportions of inherited zircons in certain samples with U–Pb ages of 627–992 Ma indicate the involvement of lower–middle Neoproterozoic crustal materials during magma crystallization through wall-rock contamination, which resulted in the wide range of isotopic compositions. Underplating of mantle-derived magma may have provided the thermal energy for partial melting of the upper Paleoproterozoic and lower Mesoproterozoic basements, thereby generating these late Triassic granites. The lack of positive <i>ε</i><sub>Hf</sub>(<i>t</i>) values and high <i>δ</i><sup>18</sup>O<sub>Zrc</sub> values indicate that the contribution of mantle-derived magmas to these granites may be insignificant.
DOI: 10.6084/m9.figshare.1290934.v1
title: Origin of Triassic granites in central Hunan Province, South China: constraints from zircon U–Pb ages and Hf and O isotopes

description: Triassic granites crop out extensively in central Hunan Province, South China. Representative granites include the Baimashan, Weishan, and Ziyunshan plutons. Lithologically, these granites mainly comprise biotite monzogranite, two-mica granites, hornblende-biotite granite, hornblende-biotite monzogranite, and garnet-muscovite granite. These granites have <i>in situ</i> zircon secondary ion mass spectrum U–Pb ages between 223.2 ± 3.3 and 209.3 ± 4.0 Ma, indicating that they likely formed predominantly in the Late Triassic. These granitic plutons have similar zircon Hf and O isotopic compositions, with <i>ε</i><sub>Hf</sub>(<i>t</i>) values of −0.8 to −9.0, two-stage depleted mantle model ages (<i>T</i><sub>DM2</sub>) of 1.81–1.31 Ga, and weighted mean of <i>δ</i><sup>18</sup>O<sub>Zrc</sub> values of 8.53 ± 0.58‰ to 9.12 ± 0.28‰. Combined with U–Pb dating and Hf isotopic data, the elevated and variable <i>δ</i><sup>18</sup>O and <i>ε</i><sub>Hf</sub>(<i>t</i>) values of the individual granites indicate that these Triassic granites were likely produced by partial melting of upper Paleoproterozoic to lower Mesoproterozoic metasedimentary rocks and are S-type granites. The variable proportions of inherited zircons in certain samples with U–Pb ages of 627–992 Ma indicate the involvement of lower–middle Neoproterozoic crustal materials during magma crystallization through wall-rock contamination, which resulted in the wide range of isotopic compositions. Underplating of mantle-derived magma may have provided the thermal energy for partial melting of the upper Paleoproterozoic and lower Mesoproterozoic basements, thereby generating these late Triassic granites. The lack of positive <i>ε</i><sub>Hf</sub>(<i>t</i>) values and high <i>δ</i><sup>18</sup>O<sub>Zrc</sub> values indicate that the contribution of mantle-derived magmas to these granites may be insignificant.
DOI: 10.6084/m9.figshare.1291010
title: Taxonomical reappraisal of Cathayornithidae (Aves: Enantiornithes)

description: A complete redescription of <i>Cathayornis caudatus</i> Hou, 1997 is provided based on new information from a resin cast of the holotype, leading to reinterpretation of many morphological features of this initially poorly diagnosed taxon. Detailed comparisons across various specimens referred to Cathayornithidae Zhou <i>et al.</i>, 1992 indicate that <i>Sinornis santensis</i>, <i>Cathayornis yandica</i>, <i>C. caudatus</i> and <i>Eocathayornis walkeri</i> are valid taxa, but that <i>C. chabuensis</i> should be regarded as a <i>nomen dubium</i>. The holotype and referred specimens of <i>C. chabuensis</i> differ significantly in morphology, indicating that they do not belong to the same species. A comprehensive phylogenetic analysis targeted at Mesozoic birds reveals that neither Cathayornithidae Zhou <i>et al.</i>, 1992 nor <i>Cathayornis</i> Zhou <i>et al.</i>, 1992 are monophyletic, and that <i>C. yandica</i> can be regarded as the only species in a monospecific Cathayornithidae. The holotype of ‘<i>C. caudatus</i>’ is assigned to the genus <i>Houornis</i> gen. nov., and a taxonomic reassessment of other ‘cathayornithids’ is presented. http://zoobank.org/urn:lsid:zoobank.org:pub:0B1A404A-CC6A-4609-8CC5-C0DD62983C9A
DOI: 10.6084/m9.figshare.1291010.v1
title: Taxonomical reappraisal of Cathayornithidae (Aves: Enantiornithes)

description: A complete redescription of <i>Cathayornis caudatus</i> Hou, 1997 is provided based on new information from a resin cast of the holotype, leading to reinterpretation of many morphological features of this initially poorly diagnosed taxon. Detailed comparisons across various specimens referred to Cathayornithidae Zhou <i>et al.</i>, 1992 indicate that <i>Sinornis santensis</i>, <i>Cathayornis yandica</i>, <i>C. caudatus</i> and <i>Eocathayornis walkeri</i> are valid taxa, but that <i>C. chabuensis</i> should be regarded as a <i>nomen dubium</i>. The holotype and referred specimens of <i>C. chabuensis</i> differ significantly in morphology, indicating that they do not belong to the same species. A comprehensive phylogenetic analysis targeted at Mesozoic birds reveals that neither Cathayornithidae Zhou <i>et al.</i>, 1992 nor <i>Cathayornis</i> Zhou <i>et al.</i>, 1992 are monophyletic, and that <i>C. yandica</i> can be regarded as the only species in a monospecific Cathayornithidae. The holotype of ‘<i>C. caudatus</i>’ is assigned to the genus <i>Houornis</i> gen. nov., and a taxonomic reassessment of other ‘cathayornithids’ is presented. http://zoobank.org/urn:lsid:zoobank.org:pub:0B1A404A-CC6A-4609-8CC5-C0DD62983C9A
DOI: 10.6084/m9.figshare.1291202
title: Characterization of TAZ domains important for the induction of breast cancer stem cell properties and tumorigenesis

description: The Hippo pathway is an evolutionarily conserved regulator of tissue growth and cell fate during development and regeneration. Conversely, deregulation of the Hippo pathway has been reported in several malignancies. Here, we used integrative functional genomics approaches to identify TAZ, a transcription co-activator and key downstream effector of the Hippo pathway, as an essential driver for the propagation of TNBC malignant phenotype. We further showed in non-transformed human mammary basal epithelial cells that expression of constitutively active TAZ confers cancer stem cell (CSC) traits that are dependent on the TAZ and TEAD interacting domains. In addition, to gain a better understanding of how TAZ functions, we performed genetic-function analysis of TAZ. Significantly, we identified that both the WW and transcriptional activation domains of TAZ are critical for the induced CSC properties as well as tumorigenic potential as manifested in vitro and in human breast cancer xenograft in vivo. Collectively, our data suggest that pharmacological inhibition of TAZ activity may provide a novel means of targeting and eliminating breast CSCs.
DOI: 10.6084/m9.figshare.1291202.v1
title: Characterization of TAZ domains important for the induction of breast cancer stem cell properties and tumorigenesis

description: The Hippo pathway is an evolutionarily conserved regulator of tissue growth and cell fate during development and regeneration. Conversely, deregulation of the Hippo pathway has been reported in several malignancies. Here, we used integrative functional genomics approaches to identify TAZ, a transcription co-activator and key downstream effector of the Hippo pathway, as an essential driver for the propagation of TNBC malignant phenotype. We further showed in non-transformed human mammary basal epithelial cells that expression of constitutively active TAZ confers cancer stem cell (CSC) traits that are dependent on the TAZ and TEAD interacting domains. In addition, to gain a better understanding of how TAZ functions, we performed genetic-function analysis of TAZ. Significantly, we identified that both the WW and transcriptional activation domains of TAZ are critical for the induced CSC properties as well as tumorigenic potential as manifested in vitro and in human breast cancer xenograft in vivo. Collectively, our data suggest that pharmacological inhibition of TAZ activity may provide a novel means of targeting and eliminating breast CSCs.
DOI: 10.6084/m9.figshare.1291202.v2
title: Characterization of TAZ domains important for the induction of breast cancer stem cell properties and tumorigenesis

description: The Hippo pathway is an evolutionarily conserved regulator of tissue growth and cell fate during development and regeneration. Conversely, deregulation of the Hippo pathway has been reported in several malignancies. Here, we used integrative functional genomics approaches to identify TAZ, a transcription co-activator and key downstream effector of the Hippo pathway, as an essential driver for the propagation of TNBC malignant phenotype. We further showed in non-transformed human mammary basal epithelial cells that expression of constitutively active TAZ confers cancer stem cell (CSC) traits that are dependent on the TAZ and TEAD interacting domains. In addition, to gain a better understanding of how TAZ functions, we performed genetic-function analysis of TAZ. Significantly, we identified that both the WW and transcriptional activation domains of TAZ are critical for the induced CSC properties as well as tumorigenic potential as manifested in vitro and in human breast cancer xenograft in vivo. Collectively, our data suggest that pharmacological inhibition of TAZ activity may provide a novel means of targeting and eliminating breast CSCs.
DOI: 10.6084/m9.figshare.1291202.v3
title: Characterization of TAZ domains important for the induction of breast cancer stem cell properties and tumorigenesis

description: The Hippo pathway is an evolutionarily conserved regulator of tissue growth and cell fate during development and regeneration. Conversely, deregulation of the Hippo pathway has been reported in several malignancies. Here, we used integrative functional genomics approaches to identify TAZ, a transcription co-activator and key downstream effector of the Hippo pathway, as an essential driver for the propagation of TNBC malignant phenotype. We further showed in non-transformed human mammary basal epithelial cells that expression of constitutively active TAZ confers cancer stem cell (CSC) traits that are dependent on the TAZ and TEAD interacting domains. In addition, to gain a better understanding of how TAZ functions, we performed genetic-function analysis of TAZ. Significantly, we identified that both the WW and transcriptional activation domains of TAZ are critical for the induced CSC properties as well as tumorigenic potential as manifested in vitro and in human breast cancer xenograft in vivo. Collectively, our data suggest that pharmacological inhibition of TAZ activity may provide a novel means of targeting and eliminating breast CSCs.
DOI: 10.6084/m9.figshare.1291722
title: TXNDC17 promotes paclitaxel resistance via inducing autophagy in ovarian cancer

description: Paclitaxel is recommended as a first-line chemotherapeutic agent against ovarian cancer, but drug resistance becomes a major limitation of its success clinically. The key molecule or mechanism associated with paclitaxel resistance in ovarian cancer still remains unclear. Here, we showed that TXNDC17 screened from 356 differentially expressed proteins by LC-MS/MS label-free quantitative proteomics was more highly expressed in paclitaxel-resistant ovarian cancer cells and tissues, and the high expression of TXNDC17 was associated with poorer prognostic factors and exhibited shortened survival in 157 ovarian cancer patients. Moreover, paclitaxel exposure induced upregulation of TXNDC17 and BECN1 expression, increase of autophagosome formation, and autophagic flux that conferred cytoprotection for ovarian cancer cells from paclitaxel. <i>TXNDC17</i> inhibition by siRNA or enforced overexpression by a pcDNA3.1(+)-TXNDC17 plasmid correspondingly decreased or increased the autophagy response and paclitaxel resistance. Additionally, the downregulation of <i>BECN1</i> by siRNA attenuated the activation of autophagy and cytoprotection from paclitaxel induced by TXNDC17 overexpression in ovarian cancer cells. Thus, our findings suggest that TXNDC17, through participation of BECN1, induces autophagy and consequently results in paclitaxel resistance in ovarian cancer. TXNDC17 may be a potential predictor or target in ovarian cancer therapeutics.
DOI: 10.6084/m9.figshare.1291722.v2
title: TXNDC17 promotes paclitaxel resistance via inducing autophagy in ovarian cancer

description: Paclitaxel is recommended as a first-line chemotherapeutic agent against ovarian cancer, but drug resistance becomes a major limitation of its success clinically. The key molecule or mechanism associated with paclitaxel resistance in ovarian cancer still remains unclear. Here, we showed that TXNDC17 screened from 356 differentially expressed proteins by LC-MS/MS label-free quantitative proteomics was more highly expressed in paclitaxel-resistant ovarian cancer cells and tissues, and the high expression of TXNDC17 was associated with poorer prognostic factors and exhibited shortened survival in 157 ovarian cancer patients. Moreover, paclitaxel exposure induced upregulation of TXNDC17 and BECN1 expression, increase of autophagosome formation, and autophagic flux that conferred cytoprotection for ovarian cancer cells from paclitaxel. <i>TXNDC17</i> inhibition by siRNA or enforced overexpression by a pcDNA3.1(+)-TXNDC17 plasmid correspondingly decreased or increased the autophagy response and paclitaxel resistance. Additionally, the downregulation of <i>BECN1</i> by siRNA attenuated the activation of autophagy and cytoprotection from paclitaxel induced by TXNDC17 overexpression in ovarian cancer cells. Thus, our findings suggest that TXNDC17, through participation of BECN1, induces autophagy and consequently results in paclitaxel resistance in ovarian cancer. TXNDC17 may be a potential predictor or target in ovarian cancer therapeutics.