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Bioss pole2 antibodies
Pole2 Antibodies, supplied by Bioss, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pole2 antibodies/product/Bioss
Average 93 stars, based on 6 article reviews

pole2 antibodies - by Bioz Stars, 2026-06

93/100 stars

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POLE2 expression in the BLCA and its relationship with overall survival. (A&B) Random forest displaying the most important proliferation essential gene (PEG) — POLE2 among the 10 prognostic PEGs. (C-G) Comparisons of POLE2 expression between the BLCA and normal tissues from the datasets (C) GSE13507, (D) GSE37851, (E) GSE40335, (F) GSE52519 and (G) GSE65635. (H) Overall survival difference in BLCA patients with high- and low-POLE2 expression from the GSE13507 dataset. (I&J) Representative immunohistochemistry (IHC) images of POLE2 protein in (I) the BLCA tissues and (J) paired normal urothelial tissues. (K) Histogram of the IHC score revealing markedly higher protein expression of POLE2 in BLCA tissues than in normal tissues. (L) An enhanced protein level of POLE2 in the muscle-invasive BLCA compared to the non-muscle invasive BLCA suggested by the IHC assay. (M) Comparison of POLE2 protein levels between the high-grade non-muscle invasive BLCA and the low-grade non-muscle invasive using the IHC assay. (N) Comparison of POLE2 protein levels between the high-grade muscle invasive BLCA and the low-grade muscle invasive using the IHC assay. *, p <0.05; **, p <0.01; ***, p <0.001.

Journal: Journal of Cancer

Article Title: Prognostic and chemotherapeutic response prediction by proliferation essential gene signature: Investigating POLE2 in bladder cancer progression and cisplatin resistance

doi: 10.7150/jca.93023

Figure Lengend Snippet: POLE2 expression in the BLCA and its relationship with overall survival. (A&B) Random forest displaying the most important proliferation essential gene (PEG) — POLE2 among the 10 prognostic PEGs. (C-G) Comparisons of POLE2 expression between the BLCA and normal tissues from the datasets (C) GSE13507, (D) GSE37851, (E) GSE40335, (F) GSE52519 and (G) GSE65635. (H) Overall survival difference in BLCA patients with high- and low-POLE2 expression from the GSE13507 dataset. (I&J) Representative immunohistochemistry (IHC) images of POLE2 protein in (I) the BLCA tissues and (J) paired normal urothelial tissues. (K) Histogram of the IHC score revealing markedly higher protein expression of POLE2 in BLCA tissues than in normal tissues. (L) An enhanced protein level of POLE2 in the muscle-invasive BLCA compared to the non-muscle invasive BLCA suggested by the IHC assay. (M) Comparison of POLE2 protein levels between the high-grade non-muscle invasive BLCA and the low-grade non-muscle invasive using the IHC assay. (N) Comparison of POLE2 protein levels between the high-grade muscle invasive BLCA and the low-grade muscle invasive using the IHC assay. *, p <0.05; **, p <0.01; ***, p <0.001.

Article Snippet: Slides were incubated with anti-POLE2 antibodies (21146-1-AP, Proteintech, Wuhan, China, diluted 1:400) and then assessed by two pathologists.

Techniques: Expressing, Immunohistochemistry, Comparison

The effects of POLE2 knockdown on the BLCA cell stemness, proliferation, invasion and migration. (A) The relationship between the POLE2 expression and RNA stemness score (RNAss) in the BLCA. (B) POLE2 expression in the T24 cells transfected with POLE2-short hairpin RNAs (POLE2-shRNAs, including POLE2-shRNA1 and POLE2-shRNA2). (C-F) Effects of POLE2 knockdown on (C) T24 cell stemness assessed by the clonogenic assay, (D) T24 cell growth determined by the CCK-8 assay, (E) T24 cell migration distance after 48 hours transfection determined by the scratch assay, and (F) the T24 cell invasion capability. (G) Effects of POLE2 knockdown on cisplatin chemotherapy resistance. **, p <0.01.

Journal: Journal of Cancer

Article Title: Prognostic and chemotherapeutic response prediction by proliferation essential gene signature: Investigating POLE2 in bladder cancer progression and cisplatin resistance

doi: 10.7150/jca.93023

Figure Lengend Snippet: The effects of POLE2 knockdown on the BLCA cell stemness, proliferation, invasion and migration. (A) The relationship between the POLE2 expression and RNA stemness score (RNAss) in the BLCA. (B) POLE2 expression in the T24 cells transfected with POLE2-short hairpin RNAs (POLE2-shRNAs, including POLE2-shRNA1 and POLE2-shRNA2). (C-F) Effects of POLE2 knockdown on (C) T24 cell stemness assessed by the clonogenic assay, (D) T24 cell growth determined by the CCK-8 assay, (E) T24 cell migration distance after 48 hours transfection determined by the scratch assay, and (F) the T24 cell invasion capability. (G) Effects of POLE2 knockdown on cisplatin chemotherapy resistance. **, p <0.01.

Article Snippet: Slides were incubated with anti-POLE2 antibodies (21146-1-AP, Proteintech, Wuhan, China, diluted 1:400) and then assessed by two pathologists.

Techniques: Knockdown, Migration, Expressing, Transfection, Clonogenic Assay, CCK-8 Assay, Wound Healing Assay

DEPDC1B was upregulated in CCA tissues and expressed in CCA cells. (A) The expression level of DEPDC1B was detected by IHC analysis in CCA tissues and normal tissues (scale bar = 250 μm). (B) The mRNA expression of DEPDC1B in HCCC-9810, HUCCT1, QBC939, and RBE cell lines was detected by qPCR. Data were shown as mean ± SD (n = 3). ** P < 0.01, *** P < 0.001.

Journal: Frontiers in Oncology

Article Title: DEPDC1B promotes development of cholangiocarcinoma through enhancing the stability of CDK1 and regulating malignant phenotypes

doi: 10.3389/fonc.2022.842205

Figure Lengend Snippet: DEPDC1B was upregulated in CCA tissues and expressed in CCA cells. (A) The expression level of DEPDC1B was detected by IHC analysis in CCA tissues and normal tissues (scale bar = 250 μm). (B) The mRNA expression of DEPDC1B in HCCC-9810, HUCCT1, QBC939, and RBE cell lines was detected by qPCR. Data were shown as mean ± SD (n = 3). ** P < 0.01, *** P < 0.001.

Article Snippet: For immunohistochemistry (IHC) staining, sections were incubated with primary anti-DEPDC1B (Cat. #bs-14356R, BIOSS) at 4°C overnight.

Techniques: Expressing

Expression patterns of DEPDC1B in CCA tissues and normal tissues revealed in immunohistochemistry analysis.

Journal: Frontiers in Oncology

Article Title: DEPDC1B promotes development of cholangiocarcinoma through enhancing the stability of CDK1 and regulating malignant phenotypes

doi: 10.3389/fonc.2022.842205

Figure Lengend Snippet: Expression patterns of DEPDC1B in CCA tissues and normal tissues revealed in immunohistochemistry analysis.

Article Snippet: For immunohistochemistry (IHC) staining, sections were incubated with primary anti-DEPDC1B (Cat. #bs-14356R, BIOSS) at 4°C overnight.

Techniques: Expressing, Immunohistochemistry

Relationship between DEPDC1B expression and tumor characteristics in patients with CCA.

Journal: Frontiers in Oncology

Article Title: DEPDC1B promotes development of cholangiocarcinoma through enhancing the stability of CDK1 and regulating malignant phenotypes

doi: 10.3389/fonc.2022.842205

Figure Lengend Snippet: Relationship between DEPDC1B expression and tumor characteristics in patients with CCA.

Article Snippet: For immunohistochemistry (IHC) staining, sections were incubated with primary anti-DEPDC1B (Cat. #bs-14356R, BIOSS) at 4°C overnight.

Techniques: Expressing

DEPDC1B knockdown inhibited CCA development in vitro . (A, B) Cell models with or without DEPDC1B knockdown were constructed by transfecting shDEPDC1B or shCtrl. The knockdown efficiency of DEPDC1B in HCCC-9810 and QBC939 cells was assessed by qPCR (A) and Western blotting (B) . (C) MTT assay was employed to show the effects of DEPDC1B on cell proliferation of HCCC-9810 and QBC939 cells. (D) Flow cytometry was performed to detect the cell apoptosis of HCCC-9810 and QBC939 cells with or without DEPDC1B knockdown. (E) Cell-cycle distribution was estimated in HCCC-9810 and QBC939 cells with or without DEPDC1B knockdown. (F) Human Apoptosis Antibody Array was performed to detect and compare the expression of apoptosis-related proteins in HCCC-9810 cells with or without DEPDC1B knockdown. (G) The effects of DEPDC1B on the cell migration ability of HCCC-9810 and QBC939 cells were evaluated by wound healing assay. (H) Western blotting was performed to show the effects of DEPDC1B knockdown on expression of EMT-related proteins. The representative images were selected from at least three independent experiments. Data were shown as mean ± SD (n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: Frontiers in Oncology

Article Title: DEPDC1B promotes development of cholangiocarcinoma through enhancing the stability of CDK1 and regulating malignant phenotypes

doi: 10.3389/fonc.2022.842205

Figure Lengend Snippet: DEPDC1B knockdown inhibited CCA development in vitro . (A, B) Cell models with or without DEPDC1B knockdown were constructed by transfecting shDEPDC1B or shCtrl. The knockdown efficiency of DEPDC1B in HCCC-9810 and QBC939 cells was assessed by qPCR (A) and Western blotting (B) . (C) MTT assay was employed to show the effects of DEPDC1B on cell proliferation of HCCC-9810 and QBC939 cells. (D) Flow cytometry was performed to detect the cell apoptosis of HCCC-9810 and QBC939 cells with or without DEPDC1B knockdown. (E) Cell-cycle distribution was estimated in HCCC-9810 and QBC939 cells with or without DEPDC1B knockdown. (F) Human Apoptosis Antibody Array was performed to detect and compare the expression of apoptosis-related proteins in HCCC-9810 cells with or without DEPDC1B knockdown. (G) The effects of DEPDC1B on the cell migration ability of HCCC-9810 and QBC939 cells were evaluated by wound healing assay. (H) Western blotting was performed to show the effects of DEPDC1B knockdown on expression of EMT-related proteins. The representative images were selected from at least three independent experiments. Data were shown as mean ± SD (n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: For immunohistochemistry (IHC) staining, sections were incubated with primary anti-DEPDC1B (Cat. #bs-14356R, BIOSS) at 4°C overnight.

Techniques: In Vitro, Construct, Western Blot, MTT Assay, Flow Cytometry, Ab Array, Expressing, Migration, Wound Healing Assay

DEPDC1B knockdown inhibited CCA development in vivo . (A, B) In vivo imaging was performed to evaluate the tumor burden in mice of shDEPDC1B and shCtrl groups at day 61 post tumor inoculation. (C) Fourteen days post injection of HUCCT1 cells with or without DEPDC1B knockdown, the volume of tumors formed in mice was measured and calculated at indicated time intervals. (D, E) Mice were sacrificed at day 61 post injection, and the tumors were removed for collecting photos (D) and weighing (E) . (F) The expression of Ki67 in sections of xenografts was detected by IHC analysis (scale bar = 100 μm). (G) TUNEL analysis was performed in xenografts of shDEPDC1B and shCtrl groups (scale bar = 200 μm). Data were shown as mean ± SD (n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: Frontiers in Oncology

Article Title: DEPDC1B promotes development of cholangiocarcinoma through enhancing the stability of CDK1 and regulating malignant phenotypes

doi: 10.3389/fonc.2022.842205

Figure Lengend Snippet: DEPDC1B knockdown inhibited CCA development in vivo . (A, B) In vivo imaging was performed to evaluate the tumor burden in mice of shDEPDC1B and shCtrl groups at day 61 post tumor inoculation. (C) Fourteen days post injection of HUCCT1 cells with or without DEPDC1B knockdown, the volume of tumors formed in mice was measured and calculated at indicated time intervals. (D, E) Mice were sacrificed at day 61 post injection, and the tumors were removed for collecting photos (D) and weighing (E) . (F) The expression of Ki67 in sections of xenografts was detected by IHC analysis (scale bar = 100 μm). (G) TUNEL analysis was performed in xenografts of shDEPDC1B and shCtrl groups (scale bar = 200 μm). Data were shown as mean ± SD (n = 3). * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: For immunohistochemistry (IHC) staining, sections were incubated with primary anti-DEPDC1B (Cat. #bs-14356R, BIOSS) at 4°C overnight.

Techniques: In Vivo, In Vivo Imaging, Injection, Expressing, TUNEL Assay

The exploration and verification of downstream underlying DEPDC1B-induced regulation of CCA. (A) A PrimeView Human Gene Expression Array was performed to identify the differentially expressed genes (DEGs) between the shDEPDC1B and shCtrl groups of HCCC-9810 cells. (B, C) The enrichment of DEGs in the canonical signaling pathway (B) and IPA disease and function (C) was analyzed by IPA. (D) A DEPDC1B-associated interaction network constructed by IPA revealed the potential linkage between DEPDC1B and CDK1. (E) Western blotting was used to detect the expression of several selected DEGs in HCCC-9810 and QBC939 cells with or without DEPDC1B knockdown. (F) The expression of CDK1 in CCA tissues and normal tissues was evaluated by IHC analysis (scale bar = 50 μm for ×200, 20 μm for ×400). (G) The mRNA expression of CDK1 in HUCCT1, QBC939, RBE. and HCCC-9810 cell lines was detected by qPCR. The representative images were selected from at least three independent experiments. Data were shown as mean ± SD (n = 3). * P < 0.05, ** P < 0.01.

Journal: Frontiers in Oncology

Article Title: DEPDC1B promotes development of cholangiocarcinoma through enhancing the stability of CDK1 and regulating malignant phenotypes

doi: 10.3389/fonc.2022.842205

Figure Lengend Snippet: The exploration and verification of downstream underlying DEPDC1B-induced regulation of CCA. (A) A PrimeView Human Gene Expression Array was performed to identify the differentially expressed genes (DEGs) between the shDEPDC1B and shCtrl groups of HCCC-9810 cells. (B, C) The enrichment of DEGs in the canonical signaling pathway (B) and IPA disease and function (C) was analyzed by IPA. (D) A DEPDC1B-associated interaction network constructed by IPA revealed the potential linkage between DEPDC1B and CDK1. (E) Western blotting was used to detect the expression of several selected DEGs in HCCC-9810 and QBC939 cells with or without DEPDC1B knockdown. (F) The expression of CDK1 in CCA tissues and normal tissues was evaluated by IHC analysis (scale bar = 50 μm for ×200, 20 μm for ×400). (G) The mRNA expression of CDK1 in HUCCT1, QBC939, RBE. and HCCC-9810 cell lines was detected by qPCR. The representative images were selected from at least three independent experiments. Data were shown as mean ± SD (n = 3). * P < 0.05, ** P < 0.01.

Article Snippet: For immunohistochemistry (IHC) staining, sections were incubated with primary anti-DEPDC1B (Cat. #bs-14356R, BIOSS) at 4°C overnight.

Techniques: Expressing, Construct, Western Blot

DEPDC1B regulates CDK1 expression through the ubiquitin–proteasome system. (A) The protein level of CDK1 was detected in shCtrl and shDEPDC1B HUCCT1 cells upon the treatment of cyclohexane (CHX) for indicated times. (B) The UbiBrowser online tool was used for predicting the E3 ligase of CDK1. (C) The protein level of CDK1 was detected in HUCCT1 cells with or without SMURF1 overexpression upon the treatment of cyclohexane (CHX) for indicated times. (D) The regulatory effects of the CDK1 protein level by DEPDC1B knockdown or SMURF1 overexpression were evaluated with or without treatment of proteasome inhibitor MG132. (E) An immunoprecipitation assay was performed for assessing the ubiquitination modification of CDK1 in shCtrl and shDEPDC1B HUCCT1 cells. (F) The interaction between DEPDC1B and SMURF1 was detected and verified by a co-immunoprecipitation assay using the IgG or SMURF1 antibody for obtaining a protein complex. (G, H) Total lysates of CCA cells with or without DEPDC1B overexpression (G) or DEPDC1B knockdown (H) were subjected to immunoprecipitation using anti-CDK1 or anti-SMURF1, followed by Western blotting analysis using indicated antibodies. All groups of cells were treated with MG132 to inhibit the function of proteasome.

Journal: Frontiers in Oncology

Article Title: DEPDC1B promotes development of cholangiocarcinoma through enhancing the stability of CDK1 and regulating malignant phenotypes

doi: 10.3389/fonc.2022.842205

Figure Lengend Snippet: DEPDC1B regulates CDK1 expression through the ubiquitin–proteasome system. (A) The protein level of CDK1 was detected in shCtrl and shDEPDC1B HUCCT1 cells upon the treatment of cyclohexane (CHX) for indicated times. (B) The UbiBrowser online tool was used for predicting the E3 ligase of CDK1. (C) The protein level of CDK1 was detected in HUCCT1 cells with or without SMURF1 overexpression upon the treatment of cyclohexane (CHX) for indicated times. (D) The regulatory effects of the CDK1 protein level by DEPDC1B knockdown or SMURF1 overexpression were evaluated with or without treatment of proteasome inhibitor MG132. (E) An immunoprecipitation assay was performed for assessing the ubiquitination modification of CDK1 in shCtrl and shDEPDC1B HUCCT1 cells. (F) The interaction between DEPDC1B and SMURF1 was detected and verified by a co-immunoprecipitation assay using the IgG or SMURF1 antibody for obtaining a protein complex. (G, H) Total lysates of CCA cells with or without DEPDC1B overexpression (G) or DEPDC1B knockdown (H) were subjected to immunoprecipitation using anti-CDK1 or anti-SMURF1, followed by Western blotting analysis using indicated antibodies. All groups of cells were treated with MG132 to inhibit the function of proteasome.

Article Snippet: For immunohistochemistry (IHC) staining, sections were incubated with primary anti-DEPDC1B (Cat. #bs-14356R, BIOSS) at 4°C overnight.

Techniques: Expressing, Over Expression, Immunoprecipitation, Modification, Co-Immunoprecipitation Assay, Western Blot

Knockdown of CDK1 attenuated the effects of CCA cells by DEPDC1B overexpression. HUCCT1 cells transfected with control plasmids, DEPDC1B overexpression plasmids, NC(OE+KD), and simultaneous DEPDC1B overexpression plasmids, and shCDK1 were subjected to the detection of cell proliferation by Celigo cell counting assay (A) , colony formation (B) , cell apoptosis by flow cytometry (C) , cell migration by wound healing assay (D) , and cell migration by Transwell assay (E) . The representative images were selected from at least three independent experiments. Data were shown as mean ± SD (n = 3). ** P < 0.01, *** P < 0.001.

Journal: Frontiers in Oncology

Article Title: DEPDC1B promotes development of cholangiocarcinoma through enhancing the stability of CDK1 and regulating malignant phenotypes

doi: 10.3389/fonc.2022.842205

Figure Lengend Snippet: Knockdown of CDK1 attenuated the effects of CCA cells by DEPDC1B overexpression. HUCCT1 cells transfected with control plasmids, DEPDC1B overexpression plasmids, NC(OE+KD), and simultaneous DEPDC1B overexpression plasmids, and shCDK1 were subjected to the detection of cell proliferation by Celigo cell counting assay (A) , colony formation (B) , cell apoptosis by flow cytometry (C) , cell migration by wound healing assay (D) , and cell migration by Transwell assay (E) . The representative images were selected from at least three independent experiments. Data were shown as mean ± SD (n = 3). ** P < 0.01, *** P < 0.001.

Article Snippet: For immunohistochemistry (IHC) staining, sections were incubated with primary anti-DEPDC1B (Cat. #bs-14356R, BIOSS) at 4°C overnight.

Techniques: Over Expression, Transfection, Cell Counting, Flow Cytometry, Migration, Wound Healing Assay, Transwell Assay

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