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Jianwen Chen - One of the best experts on this subject based on the ideXlab platform.
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Deficiency of Mettl3 in Bladder Cancer Stem Cells Inhibits Bladder Cancer Progression and Angiogenesis
Frontiers in Cell and Developmental Biology, 2021Co-Authors: Ganping Wang, Yarong Dai, Maosheng Cheng, Gan Xiong, Xiaochen Wang, Shuang Chen, Zhi Chen, Jianwen ChenAbstract:RNA N6-methyladenosine is a key step of posttranscriptional modulation that is involved in governing gene expression. The m6A modification catalyzed by Mettl3 has been widely recognized as a critical epigenetic regulation process for tumorigenic properties in various Cancer cell lines, including Bladder Cancer. However, the in vivo function of Mettl3 in Bladder Cancer remains largely unknown. In our study, we found that ablation of Mettl3 in Bladder urothelial attenuates the oncogenesis and tumor angiogenesis of Bladder Cancer using transgenic mouse model. In addition, conditional knockout of Mettl3 in K14+ Bladder Cancer stem cell population leads to inhibition of Bladder Cancer progression. Coupled with the global transcriptome sequencing and methylated RNA immunoprecipitation sequencing results, we showed that deletion of Mettl3 leads to the suppression of tyrosine kinase endothelial (TEK) and vascular endothelial growth factor A (VEGF-A) through reduced abundance of m6A peaks on a specific region. In addition, the depletion of Mettl3 results in the decrease in both messenger RNA (mRNA) and protein levels of TEK and VEGF-A in vitro. Taken together, Mettl3-mediated m6A modification is required for the activation of TEK–VEGF-A-mediated tumor progression and angiogenesis. Our findings may provide theoretical basis for Bladder Cancer treatment targeting Mettl3.
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Deficiency of Mettl3 in Bladder Cancer Stem Cells inhibits Bladder Cancer Progression and Angiogenesis
2020Co-Authors: Ganping Wang, Yarong Dai, Maosheng Cheng, Gan Xiong, Xiaochen Wang, Shuang Chen, Zhi Chen, Jianwen ChenAbstract:Abstract Background: RNA N6-methyladenosine is a key step of post-transcriptional modulation which involves in governing gene expression. The m6A modification catalyzed by Mettl3 has been widely recognized as a critical epigenetic regulation process for tumorigenic properties in various Cancer cell lines, including Bladder Cancer. However, the in vivo function of Mettl3 in Bladder Cancer remains largely unknown. Methods: Establishment of transgenic mouse model for exploring the role and mechanisms of Mettl3 in Bladder Cancer. Coupled global transcriptome sequencing and methylated RNA immunoprecipitation sequencing is performed to identify targets modulated by Mettl3.Results: We found that ablation of Mettl3 in Bladder urothelial attenuates the oncogenesis and tumor angiogenesis of Bladder Cancer. In addition, conditional knockout of Mettl3 in K14+ Bladder Cancer stem cell population leads to inhibition of Bladder Cancer progression. And deletion of Mettl3 leads to the suppression of TEK and VEGF-A through reduced abundance of m6A peaks on specific region. Conclusions: Taken together, Mettl3-mediated m6A modification is required for the activation of TEK-VEGF-A-mediated tumor progression and angiogenesis. Our findings may provide theoretical basis for Bladder Cancer treatment targeting Mettl3.
Benkang Shi - One of the best experts on this subject based on the ideXlab platform.
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Amyloid precursor protein is overexpressed in Bladder Cancer and contributes to the malignant Bladder Cancer cell behaviors
International journal of urology : official journal of the Japanese Urological Association, 2018Co-Authors: Dongqing Zhang, Changkuo Zhou, Lijian Gao, Zhipeng Pang, Gang Yin, Benkang ShiAbstract:Objectives To investigate the expression of amyloid precursor protein in Bladder Cancer, and to study its role in malignant Bladder Cancer cell behaviors. Methods Immunohistochemistry and western blotting analysis were used to detect the amyloid precursor protein level in Bladder Cancer tissues and cell lines. The effect of amyloid precursor protein on Bladder Cancer cell proliferation, migration, invasion and cell cycle was evaluated by using small interfering ribonucleic acid. The levels of RAS, RAF, MEK, phosphorylated MEK, extracellular regulated protein kinases, phosphorylated extracellular regulated protein kinases, protein kinase B and phosphorylated protein kinase B were determined by western blot after amyloid precursor protein knockdown. The effect of amyloid precursor protein on the extracellular regulated protein kinases pathway was further evaluated using extracellular regulated protein kinases pathway agonist, ceramide C6. Results The expression of amyloid precursor protein was significantly increased in the human Bladder Cancer tissues compared with matched normal Bladder tissues. The overexpression of amyloid precursor protein was significantly associated with tumor stage, tumor size, histological grade and lymph node metastasis. The proliferation, migration and invasion of human Bladder Cancer cells were significantly inhibited by the silencing of amyloid precursor protein. In addition, knockdown of amyloid precursor protein arrested the cell cycle progression of Bladder Cancer cells in the G2/M phase. Mechanistic analysis showed that knockdown of amyloid precursor protein significantly decreased the phosphorylation of extracellular regulated protein kinases. Ceramide C6 could rescue the malignant Bladder Cancer cell behaviors inhibited by the silencing of amyloid precursor protein. Conclusions Amyloid precursor protein is upregulated in Bladder Cancer, and might be closely associated with Bladder Cancer cell growth and survival. Amyloid precursor protein could potentially be used as a therapeutic target for Bladder Cancer treatment.
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Amyloid precursor protein is overexpressed in Bladder Cancer and contributes to the malignant Bladder Cancer cell behaviors
International journal of urology : official journal of the Japanese Urological Association, 2018Co-Authors: Dongqing Zhang, Changkuo Zhou, Lijian Gao, Zhipeng Pang, Gang Yin, Benkang ShiAbstract:To investigate the expression of amyloid precursor protein in Bladder Cancer, and to study its role in malignant Bladder Cancer cell behaviors. Immunohistochemistry and western blotting analysis were used to detect the amyloid precursor protein level in Bladder Cancer tissues and cell lines. The effect of amyloid precursor protein on Bladder Cancer cell proliferation, migration, invasion and cell cycle was evaluated by using small interfering ribonucleic acid. The levels of RAS, RAF, MEK, phosphorylated MEK, extracellular regulated protein kinases, phosphorylated extracellular regulated protein kinases, protein kinase B and phosphorylated protein kinase B were determined by western blot after amyloid precursor protein knockdown. The effect of amyloid precursor protein on the extracellular regulated protein kinases pathway was further evaluated using extracellular regulated protein kinases pathway agonist, ceramide C6. The expression of amyloid precursor protein was significantly increased in the human Bladder Cancer tissues compared with matched normal Bladder tissues. The overexpression of amyloid precursor protein was significantly associated with tumor stage, tumor size, histological grade and lymph node metastasis. The proliferation, migration and invasion of human Bladder Cancer cells were significantly inhibited by the silencing of amyloid precursor protein. In addition, knockdown of amyloid precursor protein arrested the cell cycle progression of Bladder Cancer cells in the G2/M phase. Mechanistic analysis showed that knockdown of amyloid precursor protein significantly decreased the phosphorylation of extracellular regulated protein kinases. Ceramide C6 could rescue the malignant Bladder Cancer cell behaviors inhibited by the silencing of amyloid precursor protein. Amyloid precursor protein is upregulated in Bladder Cancer, and might be closely associated with Bladder Cancer cell growth and survival. Amyloid precursor protein could potentially be used as a therapeutic target for Bladder Cancer treatment. © 2018 The Japanese Urological Association.
Ganping Wang - One of the best experts on this subject based on the ideXlab platform.
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Deficiency of Mettl3 in Bladder Cancer Stem Cells Inhibits Bladder Cancer Progression and Angiogenesis
Frontiers in Cell and Developmental Biology, 2021Co-Authors: Ganping Wang, Yarong Dai, Maosheng Cheng, Gan Xiong, Xiaochen Wang, Shuang Chen, Zhi Chen, Jianwen ChenAbstract:RNA N6-methyladenosine is a key step of posttranscriptional modulation that is involved in governing gene expression. The m6A modification catalyzed by Mettl3 has been widely recognized as a critical epigenetic regulation process for tumorigenic properties in various Cancer cell lines, including Bladder Cancer. However, the in vivo function of Mettl3 in Bladder Cancer remains largely unknown. In our study, we found that ablation of Mettl3 in Bladder urothelial attenuates the oncogenesis and tumor angiogenesis of Bladder Cancer using transgenic mouse model. In addition, conditional knockout of Mettl3 in K14+ Bladder Cancer stem cell population leads to inhibition of Bladder Cancer progression. Coupled with the global transcriptome sequencing and methylated RNA immunoprecipitation sequencing results, we showed that deletion of Mettl3 leads to the suppression of tyrosine kinase endothelial (TEK) and vascular endothelial growth factor A (VEGF-A) through reduced abundance of m6A peaks on a specific region. In addition, the depletion of Mettl3 results in the decrease in both messenger RNA (mRNA) and protein levels of TEK and VEGF-A in vitro. Taken together, Mettl3-mediated m6A modification is required for the activation of TEK–VEGF-A-mediated tumor progression and angiogenesis. Our findings may provide theoretical basis for Bladder Cancer treatment targeting Mettl3.
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Deficiency of Mettl3 in Bladder Cancer Stem Cells inhibits Bladder Cancer Progression and Angiogenesis
2020Co-Authors: Ganping Wang, Yarong Dai, Maosheng Cheng, Gan Xiong, Xiaochen Wang, Shuang Chen, Zhi Chen, Jianwen ChenAbstract:Abstract Background: RNA N6-methyladenosine is a key step of post-transcriptional modulation which involves in governing gene expression. The m6A modification catalyzed by Mettl3 has been widely recognized as a critical epigenetic regulation process for tumorigenic properties in various Cancer cell lines, including Bladder Cancer. However, the in vivo function of Mettl3 in Bladder Cancer remains largely unknown. Methods: Establishment of transgenic mouse model for exploring the role and mechanisms of Mettl3 in Bladder Cancer. Coupled global transcriptome sequencing and methylated RNA immunoprecipitation sequencing is performed to identify targets modulated by Mettl3.Results: We found that ablation of Mettl3 in Bladder urothelial attenuates the oncogenesis and tumor angiogenesis of Bladder Cancer. In addition, conditional knockout of Mettl3 in K14+ Bladder Cancer stem cell population leads to inhibition of Bladder Cancer progression. And deletion of Mettl3 leads to the suppression of TEK and VEGF-A through reduced abundance of m6A peaks on specific region. Conclusions: Taken together, Mettl3-mediated m6A modification is required for the activation of TEK-VEGF-A-mediated tumor progression and angiogenesis. Our findings may provide theoretical basis for Bladder Cancer treatment targeting Mettl3.
Monika Joshi - One of the best experts on this subject based on the ideXlab platform.
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Immunotherapy in Bladder Cancer
Current molecular pharmacology, 2016Co-Authors: Monali K. Vasekar, David J. Degraff, Monika JoshiAbstract:With the advent of Bacille Calmette Guerin (BCG), Bladder Cancer was one of the earliest Cancers where the concept of immunotherapy was utilized. While this is true, recent advances in the use of immunotherapy are enabling oncologists to expand the armamentarium for the treatment of Bladder Cancer. Unacceptable side effects and failure to produce a durable response with the use of chemotherapeutic agents in Bladder Cancer has led to the evaluation of more targeted and personalized approaches. Increased understanding of the underlying carcinogenesis of Bladder Cancer, coupled with the ability to engineer targeted agents implicated in Bladder Cancer associated pathways has provided new avenues for the management of this disease. Newer immunotherapeutic approaches have generated a great deal of interest in Bladder Cancer along with other diseases. In this article we will focus on various forms of immunotherapies that may have a therapeutic potential in Bladder Cancer. We will briefly review the current status of "non-targeted" immunotherapeutic agents like BCG, interferons and interleukins in Bladder Cancer. But the main focus of this article is to discuss the emerging role of "targeted" immunotherapeutic agents like cytotoxic T cell lymphocyte associated protein-4 blocking antibody and programmed death pathway blocking antibodies in localized or metastatic Bladder Cancer.
Eva Negri - One of the best experts on this subject based on the ideXlab platform.
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Nutrition and Bladder Cancer.
Cancer causes & control : CCC, 1996Co-Authors: Caxlo La Vecchia, Eva NegriAbstract:Epidemiologic evidence on the relation between nutrition and Bladder Cancer is reviewed. A role of diet and nutrition in Bladder carcinogenisis is plausible since most substances or metabolites, including carcinogens, are excreted through the urinary tract. Ecologic studies on populations have found positive correlations between fats and oils and Bladder Cancer, but these are reflected only partly in the international differences in Bladder Cancer rates, which are systematically higher in Europe than in the United States. Ten case-control and three cohort studies of Bladder Cancer published in English between 1979 and 1994, and including some information on dietary factors, were reviewed. Of seven studies which considered various types and measures of fruit and vegetable consumption, six found a reduced risk with increasing consumption, which was more consistent for vegetables, with relative risk (RR) estimates between 0.5 and 0.7 for the highest cf the lowest consumption level. There is, therefore, suggestive evidence that a diet rich in fresh fruit and vegetables is a correlate-or an indicator-of reduced Bladder Cancer risk. No clear association emerged for other foods investigated, including meat and milk. With reference to nutrients, total fat intake was related to Bladder Cancer risk in three case-control studies, with relative risks between 1.4 and 1.7 for the highest cf the lowest consumption level. However, no relationship between fats and Bladder Cancer emerged in c cohort study on Japneese-Americans in Hawaii. No consistent association emerged between protein or carbohydrate consumption and Bladder Cancer risk. Among micronutrients, vitamin A, and particularly carotenoids, showed an inverse association with Bladder Cancer risk in four case-control studies, including one allowing for a measure of total caloric intake, but were not related consistently in two other studies. There oere only scattered and inconclusive data on vitamin C and E. Finally, two studies suggested that calcium and sodium and sodium may be related to Bladder Cancer risk. Thus, available data on diet and Bladder Cancer are still inconclusive. This is at least partly attributable to the limited number of cohort studies and the paucity of case-control studies, including satisfactorily detailed and validated dietary questionnaires. Despite these limitations, available data suggest that a diet rich in fresh fruit and vegetables, and, hence, possibly in carotenoids, is a correlate of reduced Bladder Cancer risk.