9 results on '"Yun-Teng Hu"'
Search Results
2. Figure S2 from Downregulation of SAFB Sustains the NF-κB Pathway by Targeting TAK1 during the Progression of Colorectal Cancer
- Author
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Yan-Qing Ding, Wen-Ting Liao, Guang-Wen Cao, Li Liang, Jun-Feng Qiu, Qiu-Hua Lai, Yun-Teng Hu, Yue-Long Cai, Chun-Cai Gu, Yan-Ru Chen, Wen-Ting Wei, Juan-Juan Cai, Liu-Qing He, Zhi-Yuan Xiao, Yong-Xia Wang, Shu-Yang Wang, Hui-Ying Sun, Run-Wei Yang, Ya-Ping Ye, and Hong-Li Jiao
- Abstract
Figure S2 shows that down-regulation of SAFB activated NF-κB signaling pathway
- Published
- 2023
3. Data from Downregulation of SAFB Sustains the NF-κB Pathway by Targeting TAK1 during the Progression of Colorectal Cancer
- Author
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Yan-Qing Ding, Wen-Ting Liao, Guang-Wen Cao, Li Liang, Jun-Feng Qiu, Qiu-Hua Lai, Yun-Teng Hu, Yue-Long Cai, Chun-Cai Gu, Yan-Ru Chen, Wen-Ting Wei, Juan-Juan Cai, Liu-Qing He, Zhi-Yuan Xiao, Yong-Xia Wang, Shu-Yang Wang, Hui-Ying Sun, Run-Wei Yang, Ya-Ping Ye, and Hong-Li Jiao
- Abstract
Purpose: To investigate the role and the underlying mechanism of scaffold attachment factor B (SAFB) in the progression of colorectal cancer (CRC).Experimental Design: SAFB expression was analyzed in the Cancer Outlier Profile Analysis of Oncomine and in 175 paraffin-embedded archived CRC tissues. Gene Ontology analyses were performed to explore the mechanism of SAFB in CRC progression. Western blot, RT-PCR, luciferase assay, and chromatin immunoprecipitation (ChIP) were used to detect the regulation of transforming growth factor-β–activated kinase 1 (TAK1) and NF-κB signaling by SAFB. The role of SAFB in invasion, metastasis, and angiogenesis was investigated using in vitro and in vivo assays. The relationship between SAFB and TAK1 was analyzed in CRC tissues.Results: SAFB was downregulated in CRC tissues, and low expression of SAFB was significantly associated with an aggressive phenotype and poorer survival of CRC patients. The downregulation of SAFB activated NF-κB signaling by targeting the TAK1 promoter. Ectopic expression of SAFB inhibited the development of aggressive features and metastasis of CRC cells both in vitro and in vivo. The overexpression of TAK1 could rescue the aggressive features in SAFB-overexpressed cells. Furthermore, the expression of SAFB in CRC tissues was negatively correlated with the expression of TAK1- and NF-κB–related genes.Conclusions: Our results show that SAFB regulated the activity of NF-κB signaling in CRC by targeting TAK1. This novel mechanism provides a comprehensive understanding of both SAFB and the NF-κB signaling pathway in the progression of CRC and indicates that the SAFB–TAK1–NF-κB axis is a potential target for early therapeutic intervention in CRC progression. Clin Cancer Res; 23(22); 7108–18. ©2017 AACR.
- Published
- 2023
4. Supplementary materials, methods and tables from Downregulation of SAFB Sustains the NF-κB Pathway by Targeting TAK1 during the Progression of Colorectal Cancer
- Author
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Yan-Qing Ding, Wen-Ting Liao, Guang-Wen Cao, Li Liang, Jun-Feng Qiu, Qiu-Hua Lai, Yun-Teng Hu, Yue-Long Cai, Chun-Cai Gu, Yan-Ru Chen, Wen-Ting Wei, Juan-Juan Cai, Liu-Qing He, Zhi-Yuan Xiao, Yong-Xia Wang, Shu-Yang Wang, Hui-Ying Sun, Run-Wei Yang, Ya-Ping Ye, and Hong-Li Jiao
- Abstract
Supplementary materials, methods and tables
- Published
- 2023
5. Retraction Note: TLE3 represses colorectal cancer proliferation by inhibiting MAPK and AKT signaling pathways
- Author
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Yun-Teng Hu, Sheng-Lu Jiang, Hui-Ying Sun, Yan-Mei Cui, Wen-Ting Wei, Jia-Huan Zhang, Li Liang, Xin-Xin Nian, Ying-Yue Zeng, Yanqing Ding, Mei-Rong He, Yali Zhao, Wenting Liao, Ming-Xuan Li, Jun-Feng Qiu, Meng Wang, Yue-Long Cai, Run-Wei Yang, and Yu-Ping Quan
- Subjects
MAPK/ERK pathway ,Cancer Research ,Cell growth ,Cellular differentiation ,Wnt signaling pathway ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Cell cycle ,Biology ,medicine.disease_cause ,digestive system diseases ,Retraction Note ,Real-time polymerase chain reaction ,Oncology ,Cancer research ,medicine ,Carcinogenesis ,Protein kinase B ,RC254-282 - Abstract
Transducin-like enhancer of Split3 (TLE3) serves as a transcriptional corepressor during cell differentiation and shows multiple roles in different kinds of cancers. Recently, TLE3 together with many other genes involved in Wnt/β-catenin pathway were detected hyper-methylated in colorectal cancer (CRC). However, the potential role and the underlying mechanism of TLE3 in CRC progression remain scarce. Gene expression profiles were analyzed in The Cancer Genome Atlas (TCGA) microarray dataset of 41 normal colorectal intestine tissues and 465 CRC tissues. Western blot and Real-time Quantitative PCR (RT-qPCR) were respectively performed to detect protein and mRNA expression in 8 pairs of CRC tissue and matched adjacent normal mucosa. Immunohistochemistry (IHC) was conducted to evaluate TLE3 protein expression in 105 paraffin-embedded, archived human CRC tissues from patients, whose survival data were analyzed with Kaplan-Meier method. In vitro experiments including MTT assay, colony formation assay, and soft agar formation assay were used to investigate the effects of TLE3 on CRC cell growth and proliferation. Additionally, subcutaneous tumorigenesis assay was performed in nude mice to confirm the effects of TLE3 in vivo. Furthermore, gene set enrichment analysis (GSEA) was run to explore potential mechanism of TLE3 in CRC, and then we measured the distribution of CRC cell cycle phases and apoptosis by flow cytometry, as well as the impacts of TLE3 on MAPK and AKT signaling pathways by Western blot and RT-qPCR. TLE3 was significantly down-regulated in 465 CRC tissues compared with 41 normal tissues. Both protein and mRNA expressions of TLE3 were down-regulated in CRC compared with matched adjacent normal mucosa. Lower expression of TLE3 was significantly associated with poorer survival of patients with CRC. Besides, knock down of TLE3 promoted CRC cell growth and proliferation, while overexpression of TLE3 showed suppressive effects. Furthermore, overexpression of TLE3 caused G1-S phase transition arrest, inhibition of MAPK and AKT pathways, and up-regulation of p21Cip1/WAF1 and p27Kip1. This study indicated that TLE3 repressed CRC proliferation partly through inhibition of MAPK and AKT signaling pathways, suggesting the possibility of TLE3 as a biomarker for CRC prognosis.
- Published
- 2021
6. Downregulation of SAFB Sustains the NF-κB Pathway by Targeting TAK1 during the Progression of Colorectal Cancer
- Author
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Li Liang, Zhi-Yuan Xiao, Guangwen Cao, Chun-cai Gu, Shu-Yang Wang, Ya-Ping Ye, Liuqing He, Jun-Feng Qiu, Yanqing Ding, Hui-Ying Sun, Yong-Xia Wang, Hong-Li Jiao, Yan-Ru Chen, Juanjuan Cai, Wen-Ting Wei, Yue-Long Cai, Qiuhua Lai, Yun-Teng Hu, Wenting Liao, and Run-Wei Yang
- Subjects
0301 basic medicine ,Regulation of gene expression ,Cancer Research ,Angiogenesis ,Scaffold attachment factor B ,Biology ,medicine.disease ,digestive system diseases ,Metastasis ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Oncology ,Downregulation and upregulation ,030220 oncology & carcinogenesis ,medicine ,Cancer research ,Ectopic expression ,Signal transduction ,Chromatin immunoprecipitation - Abstract
Purpose: To investigate the role and the underlying mechanism of scaffold attachment factor B (SAFB) in the progression of colorectal cancer (CRC). Experimental Design: SAFB expression was analyzed in the Cancer Outlier Profile Analysis of Oncomine and in 175 paraffin-embedded archived CRC tissues. Gene Ontology analyses were performed to explore the mechanism of SAFB in CRC progression. Western blot, RT-PCR, luciferase assay, and chromatin immunoprecipitation (ChIP) were used to detect the regulation of transforming growth factor-β–activated kinase 1 (TAK1) and NF-κB signaling by SAFB. The role of SAFB in invasion, metastasis, and angiogenesis was investigated using in vitro and in vivo assays. The relationship between SAFB and TAK1 was analyzed in CRC tissues. Results: SAFB was downregulated in CRC tissues, and low expression of SAFB was significantly associated with an aggressive phenotype and poorer survival of CRC patients. The downregulation of SAFB activated NF-κB signaling by targeting the TAK1 promoter. Ectopic expression of SAFB inhibited the development of aggressive features and metastasis of CRC cells both in vitro and in vivo. The overexpression of TAK1 could rescue the aggressive features in SAFB-overexpressed cells. Furthermore, the expression of SAFB in CRC tissues was negatively correlated with the expression of TAK1- and NF-κB–related genes. Conclusions: Our results show that SAFB regulated the activity of NF-κB signaling in CRC by targeting TAK1. This novel mechanism provides a comprehensive understanding of both SAFB and the NF-κB signaling pathway in the progression of CRC and indicates that the SAFB–TAK1–NF-κB axis is a potential target for early therapeutic intervention in CRC progression. Clin Cancer Res; 23(22); 7108–18. ©2017 AACR.
- Published
- 2017
7. RETRACTED ARTICLE: TLE3 represses colorectal cancer proliferation by inhibiting MAPK and AKT signaling pathways
- Author
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Run-Wei Yang, Jia-Huan Zhang, Yali Zhao, Yanqing Ding, Hui-Ying Sun, Meng Wang, Mei-Rong He, Ying-Yue Zeng, Li Liang, Yun-Teng Hu, Sheng-Lu Jiang, Xin-Xin Nian, Yue-Long Cai, Jun-Feng Qiu, Yan-Mei Cui, Yu-Ping Quan, Wenting Liao, Ming-Xuan Li, and Wen-Ting Wei
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,Cancer Research ,Cell growth ,Cellular differentiation ,Wnt signaling pathway ,Cell cycle ,Biology ,medicine.disease_cause ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Real-time polymerase chain reaction ,Oncology ,030220 oncology & carcinogenesis ,medicine ,Cancer research ,Carcinogenesis ,Protein kinase B - Abstract
Background Transducin-like enhancer of Split3 (TLE3) serves as a transcriptional corepressor during cell differentiation and shows multiple roles in different kinds of cancers. Recently, TLE3 together with many other genes involved in Wnt/β-catenin pathway were detected hyper-methylated in colorectal cancer (CRC). However, the potential role and the underlying mechanism of TLE3 in CRC progression remain scarce. Methods Gene expression profiles were analyzed in The Cancer Genome Atlas (TCGA) microarray dataset of 41 normal colorectal intestine tissues and 465 CRC tissues. Western blot and Real-time Quantitative PCR (RT-qPCR) were respectively performed to detect protein and mRNA expression in 8 pairs of CRC tissue and matched adjacent normal mucosa. Immunohistochemistry (IHC) was conducted to evaluate TLE3 protein expression in 105 paraffin-embedded, archived human CRC tissues from patients, whose survival data were analyzed with Kaplan-Meier method. In vitro experiments including MTT assay, colony formation assay, and soft agar formation assay were used to investigate the effects of TLE3 on CRC cell growth and proliferation. Additionally, subcutaneous tumorigenesis assay was performed in nude mice to confirm the effects of TLE3 in vivo. Furthermore, gene set enrichment analysis (GSEA) was run to explore potential mechanism of TLE3 in CRC, and then we measured the distribution of CRC cell cycle phases and apoptosis by flow cytometry, as well as the impacts of TLE3 on MAPK and AKT signaling pathways by Western blot and RT-qPCR. Results TLE3 was significantly down-regulated in 465 CRC tissues compared with 41 normal tissues. Both protein and mRNA expressions of TLE3 were down-regulated in CRC compared with matched adjacent normal mucosa. Lower expression of TLE3 was significantly associated with poorer survival of patients with CRC. Besides, knock down of TLE3 promoted CRC cell growth and proliferation, while overexpression of TLE3 showed suppressive effects. Furthermore, overexpression of TLE3 caused G1-S phase transition arrest, inhibition of MAPK and AKT pathways, and up-regulation of p21Cip1/WAF1 and p27Kip1. Conclusion This study indicated that TLE3 repressed CRC proliferation partly through inhibition of MAPK and AKT signaling pathways, suggesting the possibility of TLE3 as a biomarker for CRC prognosis.
- Published
- 2016
8. Additional file 1: Table S1. of TLE3 represses colorectal cancer proliferation by inhibiting MAPK and AKT signaling pathways
- Author
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Run-Wei Yang, Ying-Yue Zeng, Wei, Wen-Ting, Cui, Yan-Mei, Sun, Hui-Ying, Cai, Yue-Long, Nian, Xin-Xin, Yun-Teng Hu, Quan, Yu-Ping, Sheng-Lu Jiang, Wang, Meng, Zhao, Ya-Li, Qiu, Jun-Feng, Li, Ming-Xuan, Jia-Huan Zhang, He, Mei-Rong, Liang, Li, Ding, Yan-Qing, and Liao, Wen-Ting
- Abstract
Primer Sequences used for RT-qPCR (5â to 3â ). (DOCX 13 kb)
- Published
- 2016
- Full Text
- View/download PDF
9. TLE3 represses colorectal cancer proliferation by inhibiting MAPK and AKT signaling pathways.
- Author
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Run-Wei Yang, Ying-Yue Zeng, Wen-Ting Wei, Yan-Mei Cui, Hui-Ying Sun, Yue-Long Cai, Xin-Xin Nian, Yun-Teng Hu, Yu-Ping Quan, Sheng-Lu Jiang, Meng Wang, Ya-Li Zhao, Jun-Feng Qiu, Ming-Xuan Li, Jia-Huan Zhang, Mei-Rong He, Li Liang, Yan-Qing Ding, and Wen-Ting Liao
- Subjects
TRANSDUCIN ,GENETICS of colon cancer ,CANCER genetics ,GENE expression ,IMMUNOHISTOCHEMISTRY - Abstract
Background: Transducin-like enhancer of Split3 (TLE3) serves as a transcriptional corepressor during cell differentiation and shows multiple roles in different kinds of cancers. Recently, TLE3 together with many other genes involved in Wnt/β-catenin pathway were detected hyper-methylated in colorectal cancer (CRC). However, the potential role and the underlying mechanism of TLE3 in CRC progression remain scarce. Methods: Gene expression profiles were analyzed in The Cancer Genome Atlas (TCGA) microarray dataset of 41 normal colorectal intestine tissues and 465 CRC tissues. Western blot and Real-time Quantitative PCR (RT-qPCR) were respectively performed to detect protein and mRNA expression in 8 pairs of CRC tissue and matched adjacent normal mucosa. Immunohistochemistry (IHC) was conducted to evaluate TLE3 protein expression in 105 paraffin-embedded, archived human CRC tissues from patients, whose survival data were analyzed with Kaplan-Meier method. In vitro experiments including MTT assay, colony formation assay, and soft agar formation assay were used to investigate the effects of TLE3 on CRC cell growth and proliferation. Additionally, subcutaneous tumorigenesis assay was performed in nude mice to confirm the effects of TLE3 in vivo. Furthermore, gene set enrichment analysis (GSEA) was run to explore potential mechanism of TLE3 in CRC, and then we measured the distribution of CRC cell cycle phases and apoptosis by flow cytometry, as well as the impacts of TLE3 on MAPK and AKT signaling pathways by Western blot and RT-qPCR. Results: TLE3 was significantly down-regulated in 465 CRC tissues compared with 41 normal tissues. Both protein and mRNA expressions of TLE3 were down-regulated in CRC compared with matched adjacent normal mucosa. Lower expression of TLE3 was significantly associated with poorer survival of patients with CRC. Besides, knock down of TLE3 promoted CRC cell growth and proliferation, while overexpression of TLE3 showed suppressive effects. Furthermore, overexpression of TLE3 caused G1-S phase transition arrest, inhibition of MAPK and AKT pathways, and up-regulation of p21Cip1/WAF1 and p27Kip1. Conclusion: This study indicated that TLE3 repressed CRC proliferation partly through inhibition of MAPK and AKT signaling pathways, suggesting the possibility of TLE3 as a biomarker for CRC prognosis. [ABSTRACT FROM AUTHOR]
- Published
- 2016
- Full Text
- View/download PDF
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