TRIM65 supports bladder urothelial carcinoma cell aggressiveness by promoting ANXA2 ubiquitination and degradation
Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumori...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wei, Wen-Su [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2018transfer abstract |
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| Schlagwörter: |
Epithelial-mesenchymal transition |
|---|
| Umfang: |
13 |
|---|
| Übergeordnetes Werk: |
Enthalten in: GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome - Hao, Lijun ELSEVIER, 2015, an international journal providing a forum for original and pertinent contributions in cancer research, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:435 ; year:2018 ; day:28 ; month:10 ; pages:10-22 ; extent:13 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.canlet.2018.07.036 |
|---|
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ELV043863620 |
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| 520 | |a Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. | ||
| 520 | |a Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. | ||
| 650 | 7 | |a Epithelial-mesenchymal transition |2 Elsevier | |
| 650 | 7 | |a Urothelial carcinoma of bladder |2 Elsevier | |
| 650 | 7 | |a Annexin A2 |2 Elsevier | |
| 650 | 7 | |a Metastasis |2 Elsevier | |
| 650 | 7 | |a TRIM65 |2 Elsevier | |
| 700 | 1 | |a Chen, Xin |4 oth | |
| 700 | 1 | |a Guo, Li-Yi |4 oth | |
| 700 | 1 | |a Li, Xiang-Dong |4 oth | |
| 700 | 1 | |a Deng, Ming-Hui |4 oth | |
| 700 | 1 | |a Yuan, Gang- Jun |4 oth | |
| 700 | 1 | |a He, Le-Ye |4 oth | |
| 700 | 1 | |a Li, Yong-Hong |4 oth | |
| 700 | 1 | |a Zhang, Zhi-Lin |4 oth | |
| 700 | 1 | |a Jiang, Li-Juan |4 oth | |
| 700 | 1 | |a Chen, Ri-Xin |4 oth | |
| 700 | 1 | |a Ma, Xiao-Dan |4 oth | |
| 700 | 1 | |a Wei, Shi |4 oth | |
| 700 | 1 | |a Ma, Ning-Fang |4 oth | |
| 700 | 1 | |a Liu, Zhuo-Wei |4 oth | |
| 700 | 1 | |a Luo, Jun-Hang |4 oth | |
| 700 | 1 | |a Zhou, Fang-Jian |4 oth | |
| 700 | 1 | |a Xie, Dan |4 oth | |
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10.1016/j.canlet.2018.07.036 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000990.pica (DE-627)ELV043863620 (ELSEVIER)S0304-3835(18)30500-7 DE-627 ger DE-627 rakwb eng 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl Wei, Wen-Su verfasserin aut TRIM65 supports bladder urothelial carcinoma cell aggressiveness by promoting ANXA2 ubiquitination and degradation 2018transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. Epithelial-mesenchymal transition Elsevier Urothelial carcinoma of bladder Elsevier Annexin A2 Elsevier Metastasis Elsevier TRIM65 Elsevier Chen, Xin oth Guo, Li-Yi oth Li, Xiang-Dong oth Deng, Ming-Hui oth Yuan, Gang- Jun oth He, Le-Ye oth Li, Yong-Hong oth Zhang, Zhi-Lin oth Jiang, Li-Juan oth Chen, Ri-Xin oth Ma, Xiao-Dan oth Wei, Shi oth Ma, Ning-Fang oth Liu, Zhuo-Wei oth Luo, Jun-Hang oth Zhou, Fang-Jian oth Xie, Dan oth Enthalten in Elsevier Science Hao, Lijun ELSEVIER GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome 2015 an international journal providing a forum for original and pertinent contributions in cancer research Amsterdam [u.a.] (DE-627)ELV013094742 volume:435 year:2018 day:28 month:10 pages:10-22 extent:13 https://doi.org/10.1016/j.canlet.2018.07.036 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_40 51.00 Werkstoffkunde: Allgemeines VZ 51.32 Werkstoffmechanik VZ AR 435 2018 28 1028 10-22 13 |
| spelling |
10.1016/j.canlet.2018.07.036 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000990.pica (DE-627)ELV043863620 (ELSEVIER)S0304-3835(18)30500-7 DE-627 ger DE-627 rakwb eng 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl Wei, Wen-Su verfasserin aut TRIM65 supports bladder urothelial carcinoma cell aggressiveness by promoting ANXA2 ubiquitination and degradation 2018transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. Epithelial-mesenchymal transition Elsevier Urothelial carcinoma of bladder Elsevier Annexin A2 Elsevier Metastasis Elsevier TRIM65 Elsevier Chen, Xin oth Guo, Li-Yi oth Li, Xiang-Dong oth Deng, Ming-Hui oth Yuan, Gang- Jun oth He, Le-Ye oth Li, Yong-Hong oth Zhang, Zhi-Lin oth Jiang, Li-Juan oth Chen, Ri-Xin oth Ma, Xiao-Dan oth Wei, Shi oth Ma, Ning-Fang oth Liu, Zhuo-Wei oth Luo, Jun-Hang oth Zhou, Fang-Jian oth Xie, Dan oth Enthalten in Elsevier Science Hao, Lijun ELSEVIER GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome 2015 an international journal providing a forum for original and pertinent contributions in cancer research Amsterdam [u.a.] (DE-627)ELV013094742 volume:435 year:2018 day:28 month:10 pages:10-22 extent:13 https://doi.org/10.1016/j.canlet.2018.07.036 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_40 51.00 Werkstoffkunde: Allgemeines VZ 51.32 Werkstoffmechanik VZ AR 435 2018 28 1028 10-22 13 |
| allfields_unstemmed |
10.1016/j.canlet.2018.07.036 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000990.pica (DE-627)ELV043863620 (ELSEVIER)S0304-3835(18)30500-7 DE-627 ger DE-627 rakwb eng 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl Wei, Wen-Su verfasserin aut TRIM65 supports bladder urothelial carcinoma cell aggressiveness by promoting ANXA2 ubiquitination and degradation 2018transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. Epithelial-mesenchymal transition Elsevier Urothelial carcinoma of bladder Elsevier Annexin A2 Elsevier Metastasis Elsevier TRIM65 Elsevier Chen, Xin oth Guo, Li-Yi oth Li, Xiang-Dong oth Deng, Ming-Hui oth Yuan, Gang- Jun oth He, Le-Ye oth Li, Yong-Hong oth Zhang, Zhi-Lin oth Jiang, Li-Juan oth Chen, Ri-Xin oth Ma, Xiao-Dan oth Wei, Shi oth Ma, Ning-Fang oth Liu, Zhuo-Wei oth Luo, Jun-Hang oth Zhou, Fang-Jian oth Xie, Dan oth Enthalten in Elsevier Science Hao, Lijun ELSEVIER GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome 2015 an international journal providing a forum for original and pertinent contributions in cancer research Amsterdam [u.a.] (DE-627)ELV013094742 volume:435 year:2018 day:28 month:10 pages:10-22 extent:13 https://doi.org/10.1016/j.canlet.2018.07.036 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_40 51.00 Werkstoffkunde: Allgemeines VZ 51.32 Werkstoffmechanik VZ AR 435 2018 28 1028 10-22 13 |
| allfieldsGer |
10.1016/j.canlet.2018.07.036 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000990.pica (DE-627)ELV043863620 (ELSEVIER)S0304-3835(18)30500-7 DE-627 ger DE-627 rakwb eng 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl Wei, Wen-Su verfasserin aut TRIM65 supports bladder urothelial carcinoma cell aggressiveness by promoting ANXA2 ubiquitination and degradation 2018transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. Epithelial-mesenchymal transition Elsevier Urothelial carcinoma of bladder Elsevier Annexin A2 Elsevier Metastasis Elsevier TRIM65 Elsevier Chen, Xin oth Guo, Li-Yi oth Li, Xiang-Dong oth Deng, Ming-Hui oth Yuan, Gang- Jun oth He, Le-Ye oth Li, Yong-Hong oth Zhang, Zhi-Lin oth Jiang, Li-Juan oth Chen, Ri-Xin oth Ma, Xiao-Dan oth Wei, Shi oth Ma, Ning-Fang oth Liu, Zhuo-Wei oth Luo, Jun-Hang oth Zhou, Fang-Jian oth Xie, Dan oth Enthalten in Elsevier Science Hao, Lijun ELSEVIER GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome 2015 an international journal providing a forum for original and pertinent contributions in cancer research Amsterdam [u.a.] (DE-627)ELV013094742 volume:435 year:2018 day:28 month:10 pages:10-22 extent:13 https://doi.org/10.1016/j.canlet.2018.07.036 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_40 51.00 Werkstoffkunde: Allgemeines VZ 51.32 Werkstoffmechanik VZ AR 435 2018 28 1028 10-22 13 |
| allfieldsSound |
10.1016/j.canlet.2018.07.036 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000990.pica (DE-627)ELV043863620 (ELSEVIER)S0304-3835(18)30500-7 DE-627 ger DE-627 rakwb eng 610 VZ 600 690 VZ 51.00 bkl 51.32 bkl Wei, Wen-Su verfasserin aut TRIM65 supports bladder urothelial carcinoma cell aggressiveness by promoting ANXA2 ubiquitination and degradation 2018transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. Epithelial-mesenchymal transition Elsevier Urothelial carcinoma of bladder Elsevier Annexin A2 Elsevier Metastasis Elsevier TRIM65 Elsevier Chen, Xin oth Guo, Li-Yi oth Li, Xiang-Dong oth Deng, Ming-Hui oth Yuan, Gang- Jun oth He, Le-Ye oth Li, Yong-Hong oth Zhang, Zhi-Lin oth Jiang, Li-Juan oth Chen, Ri-Xin oth Ma, Xiao-Dan oth Wei, Shi oth Ma, Ning-Fang oth Liu, Zhuo-Wei oth Luo, Jun-Hang oth Zhou, Fang-Jian oth Xie, Dan oth Enthalten in Elsevier Science Hao, Lijun ELSEVIER GW26-e0273 Relationship between thrombelastography test and routine platelet parameters in patients with acute coronary syndrome 2015 an international journal providing a forum for original and pertinent contributions in cancer research Amsterdam [u.a.] (DE-627)ELV013094742 volume:435 year:2018 day:28 month:10 pages:10-22 extent:13 https://doi.org/10.1016/j.canlet.2018.07.036 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_11 GBV_ILN_40 51.00 Werkstoffkunde: Allgemeines VZ 51.32 Werkstoffmechanik VZ AR 435 2018 28 1028 10-22 13 |
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trim65 supports bladder urothelial carcinoma cell aggressiveness by promoting anxa2 ubiquitination and degradation |
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TRIM65 supports bladder urothelial carcinoma cell aggressiveness by promoting ANXA2 ubiquitination and degradation |
| abstract |
Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. |
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Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. |
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Clinically, most of human urothelial carcinoma of the bladder (UCB)-related deaths result from tumor metastasis, but the underlying molecular mechanisms are largely unknown. Recently, a growing number of tripartite motif (TRIM) family members have been suggested to be important regulators for tumorigenesis. However, the impact of most TRIM members on UCB pathogenesis is unclear. In this study, TRIM65 was first screened as an important oncogenic factor of UCB from the Cancer Genome Atlas (TCGA) database and was validated by a large cohort of clinical UCB tissues. By in vitro and in vivo experiments, we demonstrated that TRIM65 promotes UCB cell invasive and metastatic capacities. Notably, we showed that TRIM65 modulates cytoskeleton rearrangement and induces UCB cells epithelial-mesenchymal transition by the ubiquitination of ANXA2, ultimately leading to an enhanced invasiveness of UCB cells. Importantly, UCBs with high expression of TRIM65 and low expression of ANXA2 showed the poorest outcome. Collectively, our results suggest that the overexpression of TRIM65 has an essential oncogenic role via ubiquitination of ANXA2 in UCB pathogenesis, and that such could be used as a novel prognostic marker and/or therapeutic target for UCB. |
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Chen, Xin Guo, Li-Yi Li, Xiang-Dong Deng, Ming-Hui Yuan, Gang- Jun He, Le-Ye Li, Yong-Hong Zhang, Zhi-Lin Jiang, Li-Juan Chen, Ri-Xin Ma, Xiao-Dan Wei, Shi Ma, Ning-Fang Liu, Zhuo-Wei Luo, Jun-Hang Zhou, Fang-Jian Xie, Dan |
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