shrna targeting usp22 Search Results


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  • 88
    Santa Cruz Biotechnology shrna lentiviral particles
    Shrna Lentiviral Particles, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Revvity Signals usp22 shrna
    (A) Female heterozygous mice with human <t>USP22</t> in the Rosa26 locus (Rosa26-Lox-Stop-Lox(3XFLAGUSP22)) were crossed with male prostate-specific probasin cre recombinase mice (PB-Cre4) to produce offspring with no expression of hUSP22 (WT) or with expression of hUSP22 (PbCre/USP22). Mice were aged at least 12 months and their prostate lobes were micro-dissected to detect expression of hUSP22 RNA (WT N=9; Pb-Cre/USP22 N=11). Student’s t-test. (B) The prostate lobes of WT and PbCre/USP22 mice aged at least 12 months underwent IHC analysis for Ki67. Representative images are shown at 40X and quantitative analysis are shown to the right (WT N=9; Pb-Cre/USP22 N=10). Student’s t-test. (C) Mouse adult fibroblasts (MAFs) from a male heterozygous mouse with human USP22 in the Rosa26 locus (Rosa26-Lox-Stop-Lox(3XFLAGUSP22)) were immortalized and then transduced with GFP control (GFP) or cre recombinase (hUSP22) to induce expression of hUSP22. (D) GFP or hUSP22 MAFs were plated for proliferation or survival assays and were treated with vehicle (N=5) or 5Gy irradiation (N=4) and measured using pico green fluorescence on Day 0, 3, and 6. Survival assays were plated and then treated on Day 0 with the designated dose of IR (N=6). (E) GFP or hUSP22 MAFs were plated for survival (N=3) or caspase-3 activity assays/western blot and treated with the indicated dose of cisplatin on Day 0. Student’s t-test. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001
    Usp22 Shrna, supplied by Revvity Signals, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Ribobio co usp22 sirna
    <t>USP22</t> was upregulated in OS tissues and cell lines. (A, B) The mRNA and protein expression levels of USP22 were markedly increased in OS tissues compared with the corresponding normal tissues. (C, D) The expression of USP22 was much higher in the OS cell lines U2OS and MG-63 than in the osteoblastic cell line hFOB at both mRNA and protein levels. * p < 0.05.
    Usp22 Sirna, supplied by Ribobio co, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/usp22 sirna/product/Ribobio co
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    86
    Santa Cruz Biotechnology shrna targeting usp22
    <t>USP22</t> was upregulated in OS tissues and cell lines. (A, B) The mRNA and protein expression levels of USP22 were markedly increased in OS tissues compared with the corresponding normal tissues. (C, D) The expression of USP22 was much higher in the OS cell lines U2OS and MG-63 than in the osteoblastic cell line hFOB at both mRNA and protein levels. * p < 0.05.
    Shrna Targeting Usp22, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Obio Technology Corp Ltd usp22 small interfering rna
    <t>USP22</t> was upregulated in OS tissues and cell lines. (A, B) The mRNA and protein expression levels of USP22 were markedly increased in OS tissues compared with the corresponding normal tissues. (C, D) The expression of USP22 was much higher in the OS cell lines U2OS and MG-63 than in the osteoblastic cell line hFOB at both mRNA and protein levels. * p < 0.05.
    Usp22 Small Interfering Rna, supplied by Obio Technology Corp Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    (A) Female heterozygous mice with human USP22 in the Rosa26 locus (Rosa26-Lox-Stop-Lox(3XFLAGUSP22)) were crossed with male prostate-specific probasin cre recombinase mice (PB-Cre4) to produce offspring with no expression of hUSP22 (WT) or with expression of hUSP22 (PbCre/USP22). Mice were aged at least 12 months and their prostate lobes were micro-dissected to detect expression of hUSP22 RNA (WT N=9; Pb-Cre/USP22 N=11). Student’s t-test. (B) The prostate lobes of WT and PbCre/USP22 mice aged at least 12 months underwent IHC analysis for Ki67. Representative images are shown at 40X and quantitative analysis are shown to the right (WT N=9; Pb-Cre/USP22 N=10). Student’s t-test. (C) Mouse adult fibroblasts (MAFs) from a male heterozygous mouse with human USP22 in the Rosa26 locus (Rosa26-Lox-Stop-Lox(3XFLAGUSP22)) were immortalized and then transduced with GFP control (GFP) or cre recombinase (hUSP22) to induce expression of hUSP22. (D) GFP or hUSP22 MAFs were plated for proliferation or survival assays and were treated with vehicle (N=5) or 5Gy irradiation (N=4) and measured using pico green fluorescence on Day 0, 3, and 6. Survival assays were plated and then treated on Day 0 with the designated dose of IR (N=6). (E) GFP or hUSP22 MAFs were plated for survival (N=3) or caspase-3 activity assays/western blot and treated with the indicated dose of cisplatin on Day 0. Student’s t-test. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

    Journal: Cancer research

    Article Title: USP22 functions as an oncogenic driver in prostate cancer by regulating cell proliferation and DNA repair

    doi: 10.1158/0008-5472.CAN-19-1033

    Figure Lengend Snippet: (A) Female heterozygous mice with human USP22 in the Rosa26 locus (Rosa26-Lox-Stop-Lox(3XFLAGUSP22)) were crossed with male prostate-specific probasin cre recombinase mice (PB-Cre4) to produce offspring with no expression of hUSP22 (WT) or with expression of hUSP22 (PbCre/USP22). Mice were aged at least 12 months and their prostate lobes were micro-dissected to detect expression of hUSP22 RNA (WT N=9; Pb-Cre/USP22 N=11). Student’s t-test. (B) The prostate lobes of WT and PbCre/USP22 mice aged at least 12 months underwent IHC analysis for Ki67. Representative images are shown at 40X and quantitative analysis are shown to the right (WT N=9; Pb-Cre/USP22 N=10). Student’s t-test. (C) Mouse adult fibroblasts (MAFs) from a male heterozygous mouse with human USP22 in the Rosa26 locus (Rosa26-Lox-Stop-Lox(3XFLAGUSP22)) were immortalized and then transduced with GFP control (GFP) or cre recombinase (hUSP22) to induce expression of hUSP22. (D) GFP or hUSP22 MAFs were plated for proliferation or survival assays and were treated with vehicle (N=5) or 5Gy irradiation (N=4) and measured using pico green fluorescence on Day 0, 3, and 6. Survival assays were plated and then treated on Day 0 with the designated dose of IR (N=6). (E) GFP or hUSP22 MAFs were plated for survival (N=3) or caspase-3 activity assays/western blot and treated with the indicated dose of cisplatin on Day 0. Student’s t-test. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

    Article Snippet: SMARTvector Human Inducible non-targeting mCMV-TurboGFP control shRNA or USP22 shRNA (Dharmacon) were used for inducible knockdown of USP22.

    Techniques: Expressing, Transduction, Irradiation, Fluorescence, Activity Assay, Western Blot

    (A) RNA-seq analysis was performed in LN-pLPLUC and LN-USP22hi cells, as well as LN-shCon and LN-shUSP22–4693 cells after 5 days of 1 μg/mL doxycycline treatment in biological triplicate, as shown in the PCA analysis. Cells were treated as described and immunoblotted with the indicated antisera. (B) MA plots show differential gene expression in LN-USP22hi cells compared to LN-pLPLUC (Left; Blue) and LN-shUSP22–4693 cells compared to LN-shCon (Right; Green). (C) Using normalized RNA-seq count data, GSEA was used to identify MSigDB pathways that were enriched upon USP22 depletion and de-enriched upon USP22 overexpression. A p value of <0.05 was used to determine significant enrichment. *represents cell cycle or DNA repair-related pathways. (D) Cells were plated for proliferation assays and treated with vehicle (UT) or irradiation (IR; LN-shCon and LN-shUSP22–4693 +2Gy IR (N=5); C42-shCon and C42-shUSP22–4693 +5Gy IR (N=3)). Cell numbers were measured using pico green fluorescence on Day 0, 3, and 6. Cells were treated with 1 μg/mL doxycycline every 48 hours. Relative cell number was achieved by normalizing to Day 0. 2-way ANOVA. (E) C42-shCon or C42-shUSP22–4693 cells were plated for clonogenic survival assays and treated with IR or cisplatin at the designated doses. Cells were treated with 1 μg/mL doxycycline every 2–3 days. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

    Journal: Cancer research

    Article Title: USP22 functions as an oncogenic driver in prostate cancer by regulating cell proliferation and DNA repair

    doi: 10.1158/0008-5472.CAN-19-1033

    Figure Lengend Snippet: (A) RNA-seq analysis was performed in LN-pLPLUC and LN-USP22hi cells, as well as LN-shCon and LN-shUSP22–4693 cells after 5 days of 1 μg/mL doxycycline treatment in biological triplicate, as shown in the PCA analysis. Cells were treated as described and immunoblotted with the indicated antisera. (B) MA plots show differential gene expression in LN-USP22hi cells compared to LN-pLPLUC (Left; Blue) and LN-shUSP22–4693 cells compared to LN-shCon (Right; Green). (C) Using normalized RNA-seq count data, GSEA was used to identify MSigDB pathways that were enriched upon USP22 depletion and de-enriched upon USP22 overexpression. A p value of <0.05 was used to determine significant enrichment. *represents cell cycle or DNA repair-related pathways. (D) Cells were plated for proliferation assays and treated with vehicle (UT) or irradiation (IR; LN-shCon and LN-shUSP22–4693 +2Gy IR (N=5); C42-shCon and C42-shUSP22–4693 +5Gy IR (N=3)). Cell numbers were measured using pico green fluorescence on Day 0, 3, and 6. Cells were treated with 1 μg/mL doxycycline every 48 hours. Relative cell number was achieved by normalizing to Day 0. 2-way ANOVA. (E) C42-shCon or C42-shUSP22–4693 cells were plated for clonogenic survival assays and treated with IR or cisplatin at the designated doses. Cells were treated with 1 μg/mL doxycycline every 2–3 days. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

    Article Snippet: SMARTvector Human Inducible non-targeting mCMV-TurboGFP control shRNA or USP22 shRNA (Dharmacon) were used for inducible knockdown of USP22.

    Techniques: RNA Sequencing Assay, Expressing, Over Expression, Irradiation, Fluorescence

    (A) Alterations, defined as amplification, homozygous deletion, mutation, mRNA upregulation, mRNA downregulation, or fusion, in USP22 occur in both primary and metastatic prostate adenocarcinoma from studies available in the cBioportal (Excluded are those studies with <1% alterations in USP22: Broad-Cornell 2013; CPC-GENE 2017; MSKCC-DFCI 2018); Studies with * represent those studies that include only genomic alterations (amplification, homozygous deletion, or mutation). (B) USP22 gene expression is positively correlated with AR or MYC gene expression using the cBioportal TCGA provisional prostate adenocarcinoma study (N=498). Inset represents co-occurrence (p value, Fisher Exact Test) of alterations in USP22 with MYC or AR. (C) Amplification and/or mRNA upregulation of USP22 are associated with decreased progression free survival in the TCGA provisional dataset (p=0.0459) using all complete tumors and the MSKCC Cancer Cell dataset (p=0.0342) using all complete tumors. Log rank test. (D) Using the MSKCC Cancer Cell 2010 dataset (cBioportal), USP22 expression was measured as a function of Gleason Grade. (E) USP22 alterations are most commonly amplification events or mRNA upregulation events. Left, those studies with only genomic alterations available (See * in Figure 1A). Right, those studies with both genomic and RNA alterations available. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

    Journal: Cancer research

    Article Title: USP22 functions as an oncogenic driver in prostate cancer by regulating cell proliferation and DNA repair

    doi: 10.1158/0008-5472.CAN-19-1033

    Figure Lengend Snippet: (A) Alterations, defined as amplification, homozygous deletion, mutation, mRNA upregulation, mRNA downregulation, or fusion, in USP22 occur in both primary and metastatic prostate adenocarcinoma from studies available in the cBioportal (Excluded are those studies with <1% alterations in USP22: Broad-Cornell 2013; CPC-GENE 2017; MSKCC-DFCI 2018); Studies with * represent those studies that include only genomic alterations (amplification, homozygous deletion, or mutation). (B) USP22 gene expression is positively correlated with AR or MYC gene expression using the cBioportal TCGA provisional prostate adenocarcinoma study (N=498). Inset represents co-occurrence (p value, Fisher Exact Test) of alterations in USP22 with MYC or AR. (C) Amplification and/or mRNA upregulation of USP22 are associated with decreased progression free survival in the TCGA provisional dataset (p=0.0459) using all complete tumors and the MSKCC Cancer Cell dataset (p=0.0342) using all complete tumors. Log rank test. (D) Using the MSKCC Cancer Cell 2010 dataset (cBioportal), USP22 expression was measured as a function of Gleason Grade. (E) USP22 alterations are most commonly amplification events or mRNA upregulation events. Left, those studies with only genomic alterations available (See * in Figure 1A). Right, those studies with both genomic and RNA alterations available. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

    Article Snippet: SMARTvector Human Inducible non-targeting mCMV-TurboGFP control shRNA or USP22 shRNA (Dharmacon) were used for inducible knockdown of USP22.

    Techniques: Amplification, Mutagenesis, Expressing

    (A) Ubiscan workflow and models used for analyses. LNCaP parental cells were transfected with shUSP22 or USP22. Three samples (LNCaP: parental, shUSP22, and USP22) were run as duplicate injections for a total of 6 LC-MS/MS experiments. (B) Differential ubiquitylation of histones H2A and H2B upon USP22 knockdown and overexpression compared to LNCaP parental control. (C) Ubiscan analysis demonstrates differentially ubiquitylated peptides upon USP22 overexpression and USP22 knockdown. Putative targets of USP22 differential ubiquitination designated as >1.5-fold decreased peptide ubiquitylation in LN-USP22 compared to control and >1.5-fold increased peptide ubiquitylation in LN-shUSP22 compared to parental control (Peptides denoted in purple). (D) Putative direct targets of USP22 function as determined by (C) with DNA repair-related peptides designated by inclusion in gene set enrichment analysis pathways (KEGG or Hallmark GSEA).

    Journal: Cancer research

    Article Title: USP22 functions as an oncogenic driver in prostate cancer by regulating cell proliferation and DNA repair

    doi: 10.1158/0008-5472.CAN-19-1033

    Figure Lengend Snippet: (A) Ubiscan workflow and models used for analyses. LNCaP parental cells were transfected with shUSP22 or USP22. Three samples (LNCaP: parental, shUSP22, and USP22) were run as duplicate injections for a total of 6 LC-MS/MS experiments. (B) Differential ubiquitylation of histones H2A and H2B upon USP22 knockdown and overexpression compared to LNCaP parental control. (C) Ubiscan analysis demonstrates differentially ubiquitylated peptides upon USP22 overexpression and USP22 knockdown. Putative targets of USP22 differential ubiquitination designated as >1.5-fold decreased peptide ubiquitylation in LN-USP22 compared to control and >1.5-fold increased peptide ubiquitylation in LN-shUSP22 compared to parental control (Peptides denoted in purple). (D) Putative direct targets of USP22 function as determined by (C) with DNA repair-related peptides designated by inclusion in gene set enrichment analysis pathways (KEGG or Hallmark GSEA).

    Article Snippet: SMARTvector Human Inducible non-targeting mCMV-TurboGFP control shRNA or USP22 shRNA (Dharmacon) were used for inducible knockdown of USP22.

    Techniques: Transfection, Liquid Chromatography with Mass Spectroscopy, Over Expression

    (A) Cell lysates underwent immunoprecipitation of USP22 and immunoblot analysis of XPC in LN-pLPLUC and LN-USP22hi (left), C42-pLPLUC and C42-USP22hi (middle), and GFP and hUSP22 MAFs (right). (B) Indicated cells grown in full serum were isolated for immunoblot analysis with the designated antisera. (C) Cell lysates underwent Ubitest analysis (Life Sensors) with pulldown of poly-ubiquitylated proteins, then +/− deubiquitylase (DUB) treatment, and subsequent immunoblot analysis of XPC in LN-pLPLUC and LN-USP22hi (left) and C42-pLPLUC and C42-USP22hi (right). The change in XPC levels was compared +/− DUB relative to input. The blots are a representative image from three independent experiments. (Student t-test; N=3). (D) LN-pLPLUC or LN-USP22hi cells underwent immunoblot analysis or proliferation assays 72 hours post-transfection of siControl or siXPC +/− 2Gy irradiation (N=3). Student’s t-test. (E) LN-pLPLUC and LN-USP22hi (left) and C42-pLPLUC and C42-USP22hi (right) cells were used for immunoblot analysis of chromatin tethering experiments. (F) LN-pLPLUC or LN-USP22hi, C42-pLPLUC or C42-USP22hi, LN-shCon or LN-shUSP22–4693, and C42-shCon or C42-shUSP22–4693 cells were plated for immunofluorescence analysis of XPC. A representative experiment is shown and at least three independent experiments were performed. Student’s t-test. (G) LN-pLPLUC or LN-USP22hi, C42-pLPLUC or C42-USP22hi, LN-shCon or LN-shUSP22–4693, and C42-shCon or C42-shUSP22–4693 cells were plated and immunofluorescence of XPC was analyzed 24 hours post-5Gy irradiation. A representative experiment is shown and at least three independent experiments were performed. Student’s t-test. (H) LN-shCon or shUSP22–4693 cells were treated with 10 J UV irradiation (N=3 independent experiments in technical triplicate) and cyclobutane pyrimidine dimers (CPDs) were measured by ELISA. (I) Model of study findings. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

    Journal: Cancer research

    Article Title: USP22 functions as an oncogenic driver in prostate cancer by regulating cell proliferation and DNA repair

    doi: 10.1158/0008-5472.CAN-19-1033

    Figure Lengend Snippet: (A) Cell lysates underwent immunoprecipitation of USP22 and immunoblot analysis of XPC in LN-pLPLUC and LN-USP22hi (left), C42-pLPLUC and C42-USP22hi (middle), and GFP and hUSP22 MAFs (right). (B) Indicated cells grown in full serum were isolated for immunoblot analysis with the designated antisera. (C) Cell lysates underwent Ubitest analysis (Life Sensors) with pulldown of poly-ubiquitylated proteins, then +/− deubiquitylase (DUB) treatment, and subsequent immunoblot analysis of XPC in LN-pLPLUC and LN-USP22hi (left) and C42-pLPLUC and C42-USP22hi (right). The change in XPC levels was compared +/− DUB relative to input. The blots are a representative image from three independent experiments. (Student t-test; N=3). (D) LN-pLPLUC or LN-USP22hi cells underwent immunoblot analysis or proliferation assays 72 hours post-transfection of siControl or siXPC +/− 2Gy irradiation (N=3). Student’s t-test. (E) LN-pLPLUC and LN-USP22hi (left) and C42-pLPLUC and C42-USP22hi (right) cells were used for immunoblot analysis of chromatin tethering experiments. (F) LN-pLPLUC or LN-USP22hi, C42-pLPLUC or C42-USP22hi, LN-shCon or LN-shUSP22–4693, and C42-shCon or C42-shUSP22–4693 cells were plated for immunofluorescence analysis of XPC. A representative experiment is shown and at least three independent experiments were performed. Student’s t-test. (G) LN-pLPLUC or LN-USP22hi, C42-pLPLUC or C42-USP22hi, LN-shCon or LN-shUSP22–4693, and C42-shCon or C42-shUSP22–4693 cells were plated and immunofluorescence of XPC was analyzed 24 hours post-5Gy irradiation. A representative experiment is shown and at least three independent experiments were performed. Student’s t-test. (H) LN-shCon or shUSP22–4693 cells were treated with 10 J UV irradiation (N=3 independent experiments in technical triplicate) and cyclobutane pyrimidine dimers (CPDs) were measured by ELISA. (I) Model of study findings. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001

    Article Snippet: SMARTvector Human Inducible non-targeting mCMV-TurboGFP control shRNA or USP22 shRNA (Dharmacon) were used for inducible knockdown of USP22.

    Techniques: Immunoprecipitation, Western Blot, Isolation, Transfection, Irradiation, Immunofluorescence, Enzyme-linked Immunosorbent Assay

    USP22 was upregulated in OS tissues and cell lines. (A, B) The mRNA and protein expression levels of USP22 were markedly increased in OS tissues compared with the corresponding normal tissues. (C, D) The expression of USP22 was much higher in the OS cell lines U2OS and MG-63 than in the osteoblastic cell line hFOB at both mRNA and protein levels. * p < 0.05.

    Journal: Oncology Research

    Article Title: Downregulation of Ubiquitin-Specific Protease 22 Inhibits Proliferation, Invasion, and Epithelial–Mesenchymal Transition in Osteosarcoma Cells

    doi: 10.3727/096504016X14772395226335

    Figure Lengend Snippet: USP22 was upregulated in OS tissues and cell lines. (A, B) The mRNA and protein expression levels of USP22 were markedly increased in OS tissues compared with the corresponding normal tissues. (C, D) The expression of USP22 was much higher in the OS cell lines U2OS and MG-63 than in the osteoblastic cell line hFOB at both mRNA and protein levels. * p < 0.05.

    Article Snippet: USP22 siRNA was purchased from RiboBio (Guangzhou, P.R.

    Techniques: Expressing

    Downregulation of USP22 inhibited OS cell proliferation and invasion in vitro. (A, B) USP22 downregulation in U2OS and MG-63 cells was confirmed by Western blot analysis. (C, D) USP22 downregulation significantly inhibited the proliferative ability of U2OS and MG-63 cells. (E, F) USP22 downregulation obviously reduced the number of invading U2OS and MG-63 cells. * p < 0.05.

    Journal: Oncology Research

    Article Title: Downregulation of Ubiquitin-Specific Protease 22 Inhibits Proliferation, Invasion, and Epithelial–Mesenchymal Transition in Osteosarcoma Cells

    doi: 10.3727/096504016X14772395226335

    Figure Lengend Snippet: Downregulation of USP22 inhibited OS cell proliferation and invasion in vitro. (A, B) USP22 downregulation in U2OS and MG-63 cells was confirmed by Western blot analysis. (C, D) USP22 downregulation significantly inhibited the proliferative ability of U2OS and MG-63 cells. (E, F) USP22 downregulation obviously reduced the number of invading U2OS and MG-63 cells. * p < 0.05.

    Article Snippet: USP22 siRNA was purchased from RiboBio (Guangzhou, P.R.

    Techniques: In Vitro, Western Blot

    Downregulation of USP22 inhibited OS tumor growth and metastasis in vivo. (A, B) USP22 downregulation significantly decreased the tumor volume and weight of the U2OS/USP22si group compared with the U2OS/NCsi group. (C) The number of lung nodules was obviously reduced in the U2OS/USP22si group compared with the U2OS/NCsi group. * p < 0.05.

    Journal: Oncology Research

    Article Title: Downregulation of Ubiquitin-Specific Protease 22 Inhibits Proliferation, Invasion, and Epithelial–Mesenchymal Transition in Osteosarcoma Cells

    doi: 10.3727/096504016X14772395226335

    Figure Lengend Snippet: Downregulation of USP22 inhibited OS tumor growth and metastasis in vivo. (A, B) USP22 downregulation significantly decreased the tumor volume and weight of the U2OS/USP22si group compared with the U2OS/NCsi group. (C) The number of lung nodules was obviously reduced in the U2OS/USP22si group compared with the U2OS/NCsi group. * p < 0.05.

    Article Snippet: USP22 siRNA was purchased from RiboBio (Guangzhou, P.R.

    Techniques: In Vivo

    Downregulation of USP22 inhibited the EMT process in OS cells. (A) The protein expression levels of EMT-related markers in U2OS cells were detected by Western blot. (B) The protein expression of EMT-related markers in U2OS cells was quantified by an Odyssey infrared laser imaging system. * p < 0.05.

    Journal: Oncology Research

    Article Title: Downregulation of Ubiquitin-Specific Protease 22 Inhibits Proliferation, Invasion, and Epithelial–Mesenchymal Transition in Osteosarcoma Cells

    doi: 10.3727/096504016X14772395226335

    Figure Lengend Snippet: Downregulation of USP22 inhibited the EMT process in OS cells. (A) The protein expression levels of EMT-related markers in U2OS cells were detected by Western blot. (B) The protein expression of EMT-related markers in U2OS cells was quantified by an Odyssey infrared laser imaging system. * p < 0.05.

    Article Snippet: USP22 siRNA was purchased from RiboBio (Guangzhou, P.R.

    Techniques: Expressing, Western Blot, Imaging

    Downregulation of USP22 inhibited the activation of the PI3K/Akt signaling pathway. (A) The protein expression levels of p-PI3K, PI3K, p-Akt, and Akt in U2OS cells were detected by Western blot. (B) U2OS and MG-63 cells were incubated with different concentrations of MK-2206. Cell growth was determined after 24 h of using MTT assay. (C, D) U2OS and MG-63 cells were transfected with USP22si or NCsi in the presence or absence of MK-2206 (100 nM). The Transwell assay was carried out to measure cell invasion. * p < 0.05.

    Journal: Oncology Research

    Article Title: Downregulation of Ubiquitin-Specific Protease 22 Inhibits Proliferation, Invasion, and Epithelial–Mesenchymal Transition in Osteosarcoma Cells

    doi: 10.3727/096504016X14772395226335

    Figure Lengend Snippet: Downregulation of USP22 inhibited the activation of the PI3K/Akt signaling pathway. (A) The protein expression levels of p-PI3K, PI3K, p-Akt, and Akt in U2OS cells were detected by Western blot. (B) U2OS and MG-63 cells were incubated with different concentrations of MK-2206. Cell growth was determined after 24 h of using MTT assay. (C, D) U2OS and MG-63 cells were transfected with USP22si or NCsi in the presence or absence of MK-2206 (100 nM). The Transwell assay was carried out to measure cell invasion. * p < 0.05.

    Article Snippet: USP22 siRNA was purchased from RiboBio (Guangzhou, P.R.

    Techniques: Activation Assay, Expressing, Western Blot, Incubation, MTT Assay, Transfection, Transwell Assay