An author name was incorrectly spelled as "Jen-Fang Lo." The correct spelling is "Jeng-Fan Lo." T... more An author name was incorrectly spelled as "Jen-Fang Lo." The correct spelling is "Jeng-Fan Lo." The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
PDF file - 187K, Additional methods including antibodies, oligonucleotides, reagents, plasmid and... more PDF file - 187K, Additional methods including antibodies, oligonucleotides, reagents, plasmid and lentiviral constructs, and transfection/preparation of lentivirus particles, are described.
Supplementary Data from Positive Correlations of Oct-4 and Nanog in Oral Cancer Stem-Like Cells a... more Supplementary Data from Positive Correlations of Oct-4 and Nanog in Oral Cancer Stem-Like Cells and High-Grade Oral Squamous Cell Carcinoma
Supplementary Methods, Figure Legends 1-6, Table Legend 1 from The Epithelial-Mesenchymal Transit... more Supplementary Methods, Figure Legends 1-6, Table Legend 1 from The Epithelial-Mesenchymal Transition Mediator S100A4 Maintains Cancer-Initiating Cells in Head and Neck Cancers
Advanced glycation end products (AGEs), which are highly reactive molecules resulting from persis... more Advanced glycation end products (AGEs), which are highly reactive molecules resulting from persistent high‐glucose levels, can lead to the generation of oxidative stress and cardiac complications. The carboxyl terminus of HSP70 interacting protein (CHIP) has been demonstrated to have a protective role in several diseases, including cardiac complications; however, the role in preventing AGE‐induced cardiac damages remains poorly understood. Here, we found that elevated AGE levels impaired cardiac CHIP expression in streptozotocin‐induced diabetes and high‐fat diet‐administered animals, representing AGE exposure models. We used the TUNEL assay, hematoxylin and eosin, Masson′s trichrome staining, and western blotting to prove that cardiac injuries were induced in diabetic animals and AGE‐treated cardiac cells. Interestingly, our results collectively indicated that CHIP overexpression significantly rescued the AGE‐induced cardiac injuries and promoted cell survival. Moreover, CHIP knockdown‐mediated stabilization of nuclear factor κB (NFκB) was attenuated by overexpressing CHIP in the cells. Furthermore, co‐immunoprecipitation and immunoblot assay revealed that CHIP promotes the ubiquitination and proteasomal degradation of AGE‐induced NFκB. Importantly, fluorescence microscopy, a luciferase reporter assay, electrophoretic mobility shift assay, and subcellular fractionation further demonstrated that CHIP overexpression inhibits AGE‐induced NFκB nuclear translocation, reduced its binding ability with the promoter sequences of the receptor of AGE, consequently inhibiting the translocation of the receptor AGE to the cell membrane for its proper function. Overall, our current study findings suggest that CHIP can target NFκB for ubiquitin‐mediated proteasomal degradation, and thereby potentially rescue AGE‐induced cardiac damages.
Supplementary Figures S1-S11. The co-expression profile among ALDH activity, memGrp78 and Glut3 i... more Supplementary Figures S1-S11. The co-expression profile among ALDH activity, memGrp78 and Glut3 in SAS Sphere cells and cisplatin-resistant (cisPtR) SAS cells was examined by FACS (S1); Single-cell suspension from parental SAS or sphere SAS cells was stained with CellROX Deep Red reagent and DCF (S2); Enrichment of the drug-resistant population after in vitro drug treatment (S3); ROSLow cells were sorted using DCFDA staining from SAS sphere cells (S4); Differentially expressed genes of reactive oxygen species scavenging in Parental cells and Sphere cells under 2, 3, 5, or 9 weeks of cultivation with defined serum-free selection medium were collected and analyzed (S5); Treatment of sphere cells with catalase inhibitor 3AT reduced catalase activity (S6); Combinatorial treatment of ROS scavenger inhibitor and cisplatin induces apoptosis cell death (S7); Knockdown of CAT or SOD2 gene expression diminished spheres-forming capability, stemness marker expression of HN-CICs (S8); Overexpression of CAT in HNCICs promotes stemness properties (S9); Overexpression of CAT in HNSCC under defined serum-free selection medium promotes stemness properties (S10); Cell viability of drugs treated hematopoietic stem cells (S11).
An author name was incorrectly spelled as "Jen-Fang Lo." The correct spelling is "Jeng-Fan Lo." T... more An author name was incorrectly spelled as "Jen-Fang Lo." The correct spelling is "Jeng-Fan Lo." The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
PDF file - 187K, Additional methods including antibodies, oligonucleotides, reagents, plasmid and... more PDF file - 187K, Additional methods including antibodies, oligonucleotides, reagents, plasmid and lentiviral constructs, and transfection/preparation of lentivirus particles, are described.
Supplementary Data from Positive Correlations of Oct-4 and Nanog in Oral Cancer Stem-Like Cells a... more Supplementary Data from Positive Correlations of Oct-4 and Nanog in Oral Cancer Stem-Like Cells and High-Grade Oral Squamous Cell Carcinoma
Supplementary Methods, Figure Legends 1-6, Table Legend 1 from The Epithelial-Mesenchymal Transit... more Supplementary Methods, Figure Legends 1-6, Table Legend 1 from The Epithelial-Mesenchymal Transition Mediator S100A4 Maintains Cancer-Initiating Cells in Head and Neck Cancers
Advanced glycation end products (AGEs), which are highly reactive molecules resulting from persis... more Advanced glycation end products (AGEs), which are highly reactive molecules resulting from persistent high‐glucose levels, can lead to the generation of oxidative stress and cardiac complications. The carboxyl terminus of HSP70 interacting protein (CHIP) has been demonstrated to have a protective role in several diseases, including cardiac complications; however, the role in preventing AGE‐induced cardiac damages remains poorly understood. Here, we found that elevated AGE levels impaired cardiac CHIP expression in streptozotocin‐induced diabetes and high‐fat diet‐administered animals, representing AGE exposure models. We used the TUNEL assay, hematoxylin and eosin, Masson′s trichrome staining, and western blotting to prove that cardiac injuries were induced in diabetic animals and AGE‐treated cardiac cells. Interestingly, our results collectively indicated that CHIP overexpression significantly rescued the AGE‐induced cardiac injuries and promoted cell survival. Moreover, CHIP knockdown‐mediated stabilization of nuclear factor κB (NFκB) was attenuated by overexpressing CHIP in the cells. Furthermore, co‐immunoprecipitation and immunoblot assay revealed that CHIP promotes the ubiquitination and proteasomal degradation of AGE‐induced NFκB. Importantly, fluorescence microscopy, a luciferase reporter assay, electrophoretic mobility shift assay, and subcellular fractionation further demonstrated that CHIP overexpression inhibits AGE‐induced NFκB nuclear translocation, reduced its binding ability with the promoter sequences of the receptor of AGE, consequently inhibiting the translocation of the receptor AGE to the cell membrane for its proper function. Overall, our current study findings suggest that CHIP can target NFκB for ubiquitin‐mediated proteasomal degradation, and thereby potentially rescue AGE‐induced cardiac damages.
Supplementary Figures S1-S11. The co-expression profile among ALDH activity, memGrp78 and Glut3 i... more Supplementary Figures S1-S11. The co-expression profile among ALDH activity, memGrp78 and Glut3 in SAS Sphere cells and cisplatin-resistant (cisPtR) SAS cells was examined by FACS (S1); Single-cell suspension from parental SAS or sphere SAS cells was stained with CellROX Deep Red reagent and DCF (S2); Enrichment of the drug-resistant population after in vitro drug treatment (S3); ROSLow cells were sorted using DCFDA staining from SAS sphere cells (S4); Differentially expressed genes of reactive oxygen species scavenging in Parental cells and Sphere cells under 2, 3, 5, or 9 weeks of cultivation with defined serum-free selection medium were collected and analyzed (S5); Treatment of sphere cells with catalase inhibitor 3AT reduced catalase activity (S6); Combinatorial treatment of ROS scavenger inhibitor and cisplatin induces apoptosis cell death (S7); Knockdown of CAT or SOD2 gene expression diminished spheres-forming capability, stemness marker expression of HN-CICs (S8); Overexpression of CAT in HNCICs promotes stemness properties (S9); Overexpression of CAT in HNSCC under defined serum-free selection medium promotes stemness properties (S10); Cell viability of drugs treated hematopoietic stem cells (S11).
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