FBXO22 promotes the development of hepatocellular carcinoma by regulating the ubiquitination and degradation of p21
Deregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3 ligase, is a member of the F-box protein family. However, the biological function of FBXO22 in HCC and the underlying molecular mechanisms are still unclear. In thi...
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Published in | Journal of experimental & clinical cancer research Vol. 38; no. 1; p. 101 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
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England
BioMed Central Ltd
26.02.2019
BioMed Central BMC |
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Abstract | Deregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3 ligase, is a member of the F-box protein family. However, the biological function of FBXO22 in HCC and the underlying molecular mechanisms are still unclear. In this study, we explored the role of FBXO22 in HCC and its mechanism of promoting tumor development.
We examined the expression of FBXO22 in normal liver cell lines, HCC cell lines, HCC tissue microarrays and fresh specimens. The correlation between FBXO22 and clinical features was analyzed in a retrospective study of 110 pairs of HCC tissue microarrays. Univariate and multivariate survival analyses were used to explore the prognostic value of FBXO22 in HCC. At the same time, the correlation between the FBXO22 and p21 was also studied in HCC samples. Knock-down and overexpression experiments, CHX and Mg132 intervention experiments, ubiquitination experiments, rescue experiments and nude mouse xenograft models were used to determine the potential mechanism by which FBXO22 promotes tumorigenesis in vitro and in vivo.
The expression of FBXO22 in HCC tissues was significantly higher than in normal liver tissues. The overall survival rate and disease-free survival time of patients with high expression of FBXO22 were significantly shorter than those of patients with low expression of FBXO22. The high expression of FBXO22 in HCC tissues were significantly correlated with serum AFP (p = 0. 003, Pearson's chi-squared test), tumor size (p = 0. 019, Pearson's chi-squared test) and vascular invasion (p = 0. 031, Pearson's chi-squared test). Especially, Multivariate analysis showed that tumor size and the expression of FBXO22 were independent prognostic indicator of OS (95% CI: 1.077-5.157, P<0.05). Correlation analysis also showed that FBXO22 was negatively correlated with p21 in tissue microarrays (r = - 0.3788, P<0.001, Pearson correlation) and fresh specimens (r = - 0.4037, P<0.01, Pearson correlation). Moreover, both in vitro and in vivo experiments showed that knocking down FBXO22 expression could inhibit cell proliferation, while overexpression of FBXO22 promoted tumor formation. Furthermore, we identified that FBXO22 interacts with p21 by regulating protein stability and by influencing the ubiquitination process. A knockdown of FBXO22 decreased the ubiquitylation of p21, while overexpression enhanced it.
This study uncovered a new mechanism by which FBXO22 functions as an oncogene in HCC pathogenesis and progression by mediating the ubiquitination and degradation of p21. It was also found that tumor size and the expression of FBXO22 were independent prognostic indicator of OS and the expression of FBXO22 and p21 was negatively correlated in clinical samples. Our findings present a new perspective for understanding the development of HCC, which may provide a new target for the treatment and management of this challenging cancer. |
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AbstractList | Background Deregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3 ligase, is a member of the F-box protein family. However, the biological function of FBXO22 in HCC and the underlying molecular mechanisms are still unclear. In this study, we explored the role of FBXO22 in HCC and its mechanism of promoting tumor development. Methods We examined the expression of FBXO22 in normal liver cell lines, HCC cell lines, HCC tissue microarrays and fresh specimens. The correlation between FBXO22 and clinical features was analyzed in a retrospective study of 110 pairs of HCC tissue microarrays. Univariate and multivariate survival analyses were used to explore the prognostic value of FBXO22 in HCC. At the same time, the correlation between the FBXO22 and p21 was also studied in HCC samples. Knock-down and overexpression experiments, CHX and Mg132 intervention experiments, ubiquitination experiments, rescue experiments and nude mouse xenograft models were used to determine the potential mechanism by which FBXO22 promotes tumorigenesis in vitro and in vivo. Results The expression of FBXO22 in HCC tissues was significantly higher than in normal liver tissues. The overall survival rate and disease-free survival time of patients with high expression of FBXO22 were significantly shorter than those of patients with low expression of FBXO22. The high expression of FBXO22 in HCC tissues were significantly correlated with serum AFP (p = 0. 003, Pearson's chi-squared test), tumor size (p = 0. 019, Pearson's chi-squared test) and vascular invasion (p = 0. 031, Pearson's chi-squared test). Especially, Multivariate analysis showed that tumor size and the expression of FBXO22 were independent prognostic indicator of OS (95% CI: 1.077-5.157, P<0.05). Correlation analysis also showed that FBXO22 was negatively correlated with p21 in tissue microarrays (r = - 0.3788, P<0.001, Pearson correlation) and fresh specimens (r = - 0.4037, P<0.01, Pearson correlation). Moreover, both in vitro and in vivo experiments showed that knocking down FBXO22 expression could inhibit cell proliferation, while overexpression of FBXO22 promoted tumor formation. Furthermore, we identified that FBXO22 interacts with p21 by regulating protein stability and by influencing the ubiquitination process. A knockdown of FBXO22 decreased the ubiquitylation of p21, while overexpression enhanced it. Conclusions This study uncovered a new mechanism by which FBXO22 functions as an oncogene in HCC pathogenesis and progression by mediating the ubiquitination and degradation of p21. It was also found that tumor size and the expression of FBXO22 were independent prognostic indicator of OS and the expression of FBXO22 and p21 was negatively correlated in clinical samples. Our findings present a new perspective for understanding the development of HCC, which may provide a new target for the treatment and management of this challenging cancer. Keywords: FBXO22, Ubiquitination, p21, HCC Deregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3 ligase, is a member of the F-box protein family. However, the biological function of FBXO22 in HCC and the underlying molecular mechanisms are still unclear. In this study, we explored the role of FBXO22 in HCC and its mechanism of promoting tumor development. We examined the expression of FBXO22 in normal liver cell lines, HCC cell lines, HCC tissue microarrays and fresh specimens. The correlation between FBXO22 and clinical features was analyzed in a retrospective study of 110 pairs of HCC tissue microarrays. Univariate and multivariate survival analyses were used to explore the prognostic value of FBXO22 in HCC. At the same time, the correlation between the FBXO22 and p21 was also studied in HCC samples. Knock-down and overexpression experiments, CHX and Mg132 intervention experiments, ubiquitination experiments, rescue experiments and nude mouse xenograft models were used to determine the potential mechanism by which FBXO22 promotes tumorigenesis in vitro and in vivo. The expression of FBXO22 in HCC tissues was significantly higher than in normal liver tissues. The overall survival rate and disease-free survival time of patients with high expression of FBXO22 were significantly shorter than those of patients with low expression of FBXO22. The high expression of FBXO22 in HCC tissues were significantly correlated with serum AFP (p = 0. 003, Pearson's chi-squared test), tumor size (p = 0. 019, Pearson's chi-squared test) and vascular invasion (p = 0. 031, Pearson's chi-squared test). Especially, Multivariate analysis showed that tumor size and the expression of FBXO22 were independent prognostic indicator of OS (95% CI: 1.077-5.157, P<0.05). Correlation analysis also showed that FBXO22 was negatively correlated with p21 in tissue microarrays (r = - 0.3788, P<0.001, Pearson correlation) and fresh specimens (r = - 0.4037, P<0.01, Pearson correlation). Moreover, both in vitro and in vivo experiments showed that knocking down FBXO22 expression could inhibit cell proliferation, while overexpression of FBXO22 promoted tumor formation. Furthermore, we identified that FBXO22 interacts with p21 by regulating protein stability and by influencing the ubiquitination process. A knockdown of FBXO22 decreased the ubiquitylation of p21, while overexpression enhanced it. This study uncovered a new mechanism by which FBXO22 functions as an oncogene in HCC pathogenesis and progression by mediating the ubiquitination and degradation of p21. It was also found that tumor size and the expression of FBXO22 were independent prognostic indicator of OS and the expression of FBXO22 and p21 was negatively correlated in clinical samples. Our findings present a new perspective for understanding the development of HCC, which may provide a new target for the treatment and management of this challenging cancer. Background Deregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3 ligase, is a member of the F-box protein family. However, the biological function of FBXO22 in HCC and the underlying molecular mechanisms are still unclear. In this study, we explored the role of FBXO22 in HCC and its mechanism of promoting tumor development. Methods We examined the expression of FBXO22 in normal liver cell lines, HCC cell lines, HCC tissue microarrays and fresh specimens. The correlation between FBXO22 and clinical features was analyzed in a retrospective study of 110 pairs of HCC tissue microarrays. Univariate and multivariate survival analyses were used to explore the prognostic value of FBXO22 in HCC. At the same time, the correlation between the FBXO22 and p21 was also studied in HCC samples. Knock-down and overexpression experiments, CHX and Mg132 intervention experiments, ubiquitination experiments, rescue experiments and nude mouse xenograft models were used to determine the potential mechanism by which FBXO22 promotes tumorigenesis in vitro and in vivo. Results The expression of FBXO22 in HCC tissues was significantly higher than in normal liver tissues. The overall survival rate and disease-free survival time of patients with high expression of FBXO22 were significantly shorter than those of patients with low expression of FBXO22. The high expression of FBXO22 in HCC tissues were significantly correlated with serum AFP (p = 0. 003, Pearson’s chi-squared test), tumor size (p = 0. 019, Pearson’s chi-squared test) and vascular invasion (p = 0. 031, Pearson’s chi-squared test). Especially, Multivariate analysis showed that tumor size and the expression of FBXO22 were independent prognostic indicator of OS (95% CI: 1.077–5.157, P<0.05). Correlation analysis also showed that FBXO22 was negatively correlated with p21 in tissue microarrays (r = − 0.3788, P<0.001, Pearson correlation) and fresh specimens (r = − 0.4037, P<0.01, Pearson correlation). Moreover, both in vitro and in vivo experiments showed that knocking down FBXO22 expression could inhibit cell proliferation, while overexpression of FBXO22 promoted tumor formation. Furthermore, we identified that FBXO22 interacts with p21 by regulating protein stability and by influencing the ubiquitination process. A knockdown of FBXO22 decreased the ubiquitylation of p21, while overexpression enhanced it. Conclusions This study uncovered a new mechanism by which FBXO22 functions as an oncogene in HCC pathogenesis and progression by mediating the ubiquitination and degradation of p21. It was also found that tumor size and the expression of FBXO22 were independent prognostic indicator of OS and the expression of FBXO22 and p21 was negatively correlated in clinical samples. Our findings present a new perspective for understanding the development of HCC, which may provide a new target for the treatment and management of this challenging cancer. Abstract Background Deregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3 ligase, is a member of the F-box protein family. However, the biological function of FBXO22 in HCC and the underlying molecular mechanisms are still unclear. In this study, we explored the role of FBXO22 in HCC and its mechanism of promoting tumor development. Methods We examined the expression of FBXO22 in normal liver cell lines, HCC cell lines, HCC tissue microarrays and fresh specimens. The correlation between FBXO22 and clinical features was analyzed in a retrospective study of 110 pairs of HCC tissue microarrays. Univariate and multivariate survival analyses were used to explore the prognostic value of FBXO22 in HCC. At the same time, the correlation between the FBXO22 and p21 was also studied in HCC samples. Knock-down and overexpression experiments, CHX and Mg132 intervention experiments, ubiquitination experiments, rescue experiments and nude mouse xenograft models were used to determine the potential mechanism by which FBXO22 promotes tumorigenesis in vitro and in vivo. Results The expression of FBXO22 in HCC tissues was significantly higher than in normal liver tissues. The overall survival rate and disease-free survival time of patients with high expression of FBXO22 were significantly shorter than those of patients with low expression of FBXO22. The high expression of FBXO22 in HCC tissues were significantly correlated with serum AFP (p = 0. 003, Pearson’s chi-squared test), tumor size (p = 0. 019, Pearson’s chi-squared test) and vascular invasion (p = 0. 031, Pearson’s chi-squared test). Especially, Multivariate analysis showed that tumor size and the expression of FBXO22 were independent prognostic indicator of OS (95% CI: 1.077–5.157, P<0.05). Correlation analysis also showed that FBXO22 was negatively correlated with p21 in tissue microarrays (r = − 0.3788, P<0.001, Pearson correlation) and fresh specimens (r = − 0.4037, P<0.01, Pearson correlation). Moreover, both in vitro and in vivo experiments showed that knocking down FBXO22 expression could inhibit cell proliferation, while overexpression of FBXO22 promoted tumor formation. Furthermore, we identified that FBXO22 interacts with p21 by regulating protein stability and by influencing the ubiquitination process. A knockdown of FBXO22 decreased the ubiquitylation of p21, while overexpression enhanced it. Conclusions This study uncovered a new mechanism by which FBXO22 functions as an oncogene in HCC pathogenesis and progression by mediating the ubiquitination and degradation of p21. It was also found that tumor size and the expression of FBXO22 were independent prognostic indicator of OS and the expression of FBXO22 and p21 was negatively correlated in clinical samples. Our findings present a new perspective for understanding the development of HCC, which may provide a new target for the treatment and management of this challenging cancer. BACKGROUNDDeregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3 ligase, is a member of the F-box protein family. However, the biological function of FBXO22 in HCC and the underlying molecular mechanisms are still unclear. In this study, we explored the role of FBXO22 in HCC and its mechanism of promoting tumor development.METHODSWe examined the expression of FBXO22 in normal liver cell lines, HCC cell lines, HCC tissue microarrays and fresh specimens. The correlation between FBXO22 and clinical features was analyzed in a retrospective study of 110 pairs of HCC tissue microarrays. Univariate and multivariate survival analyses were used to explore the prognostic value of FBXO22 in HCC. At the same time, the correlation between the FBXO22 and p21 was also studied in HCC samples. Knock-down and overexpression experiments, CHX and Mg132 intervention experiments, ubiquitination experiments, rescue experiments and nude mouse xenograft models were used to determine the potential mechanism by which FBXO22 promotes tumorigenesis in vitro and in vivo.RESULTSThe expression of FBXO22 in HCC tissues was significantly higher than in normal liver tissues. The overall survival rate and disease-free survival time of patients with high expression of FBXO22 were significantly shorter than those of patients with low expression of FBXO22. The high expression of FBXO22 in HCC tissues were significantly correlated with serum AFP (p = 0. 003, Pearson's chi-squared test), tumor size (p = 0. 019, Pearson's chi-squared test) and vascular invasion (p = 0. 031, Pearson's chi-squared test). Especially, Multivariate analysis showed that tumor size and the expression of FBXO22 were independent prognostic indicator of OS (95% CI: 1.077-5.157, P<0.05). Correlation analysis also showed that FBXO22 was negatively correlated with p21 in tissue microarrays (r = - 0.3788, P<0.001, Pearson correlation) and fresh specimens (r = - 0.4037, P<0.01, Pearson correlation). Moreover, both in vitro and in vivo experiments showed that knocking down FBXO22 expression could inhibit cell proliferation, while overexpression of FBXO22 promoted tumor formation. Furthermore, we identified that FBXO22 interacts with p21 by regulating protein stability and by influencing the ubiquitination process. A knockdown of FBXO22 decreased the ubiquitylation of p21, while overexpression enhanced it.CONCLUSIONSThis study uncovered a new mechanism by which FBXO22 functions as an oncogene in HCC pathogenesis and progression by mediating the ubiquitination and degradation of p21. It was also found that tumor size and the expression of FBXO22 were independent prognostic indicator of OS and the expression of FBXO22 and p21 was negatively correlated in clinical samples. Our findings present a new perspective for understanding the development of HCC, which may provide a new target for the treatment and management of this challenging cancer. Deregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3 ligase, is a member of the F-box protein family. However, the biological function of FBXO22 in HCC and the underlying molecular mechanisms are still unclear. In this study, we explored the role of FBXO22 in HCC and its mechanism of promoting tumor development. We examined the expression of FBXO22 in normal liver cell lines, HCC cell lines, HCC tissue microarrays and fresh specimens. The correlation between FBXO22 and clinical features was analyzed in a retrospective study of 110 pairs of HCC tissue microarrays. Univariate and multivariate survival analyses were used to explore the prognostic value of FBXO22 in HCC. At the same time, the correlation between the FBXO22 and p21 was also studied in HCC samples. Knock-down and overexpression experiments, CHX and Mg132 intervention experiments, ubiquitination experiments, rescue experiments and nude mouse xenograft models were used to determine the potential mechanism by which FBXO22 promotes tumorigenesis in vitro and in vivo. The expression of FBXO22 in HCC tissues was significantly higher than in normal liver tissues. The overall survival rate and disease-free survival time of patients with high expression of FBXO22 were significantly shorter than those of patients with low expression of FBXO22. The high expression of FBXO22 in HCC tissues were significantly correlated with serum AFP (p = 0. 003, Pearson's chi-squared test), tumor size (p = 0. 019, Pearson's chi-squared test) and vascular invasion (p = 0. 031, Pearson's chi-squared test). Especially, Multivariate analysis showed that tumor size and the expression of FBXO22 were independent prognostic indicator of OS (95% CI: 1.077-5.157, P<0.05). Correlation analysis also showed that FBXO22 was negatively correlated with p21 in tissue microarrays (r = - 0.3788, P<0.001, Pearson correlation) and fresh specimens (r = - 0.4037, P<0.01, Pearson correlation). Moreover, both in vitro and in vivo experiments showed that knocking down FBXO22 expression could inhibit cell proliferation, while overexpression of FBXO22 promoted tumor formation. Furthermore, we identified that FBXO22 interacts with p21 by regulating protein stability and by influencing the ubiquitination process. A knockdown of FBXO22 decreased the ubiquitylation of p21, while overexpression enhanced it. This study uncovered a new mechanism by which FBXO22 functions as an oncogene in HCC pathogenesis and progression by mediating the ubiquitination and degradation of p21. It was also found that tumor size and the expression of FBXO22 were independent prognostic indicator of OS and the expression of FBXO22 and p21 was negatively correlated in clinical samples. Our findings present a new perspective for understanding the development of HCC, which may provide a new target for the treatment and management of this challenging cancer. |
ArticleNumber | 101 |
Audience | Academic |
Author | Zhang, Bixiang Chen, Jin Wang, Chao Zhang, Zhaoqi Chu, Liang Zhang, Long Chen, Xiaoping Liang, Hui-Fang Ning, Deng Liu, Qiumeng Yu, Chengpeng |
Author_xml | – sequence: 1 givenname: Long surname: Zhang fullname: Zhang, Long organization: Department of Hepatobiliary Surgery, The First Affiliated Hospital, College of Medicine, Shihezi University, Shihezi, Xinjiang, 832008, People's Republic of China – sequence: 2 givenname: Jin surname: Chen fullname: Chen, Jin organization: Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Clinical Medicine Research Center for Hepatic Surgery of Hubei Province, Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, Hubei, 430030, People's Republic of China – sequence: 3 givenname: Deng surname: Ning fullname: Ning, Deng organization: Department of Biliary and Pancreatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People's Republic of China – sequence: 4 givenname: Qiumeng surname: Liu fullname: Liu, Qiumeng organization: Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Clinical Medicine Research Center for Hepatic Surgery of Hubei Province, Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, Hubei, 430030, People's Republic of China – sequence: 5 givenname: Chao surname: Wang fullname: Wang, Chao organization: Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Clinical Medicine Research Center for Hepatic Surgery of Hubei Province, Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, Hubei, 430030, People's Republic of China – sequence: 6 givenname: Zhaoqi surname: Zhang fullname: Zhang, Zhaoqi organization: Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Clinical Medicine Research Center for Hepatic Surgery of Hubei Province, Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, Hubei, 430030, People's Republic of China – sequence: 7 givenname: Liang surname: Chu fullname: Chu, Liang organization: Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Clinical Medicine Research Center for Hepatic Surgery of Hubei Province, Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, Hubei, 430030, People's Republic of China – sequence: 8 givenname: Chengpeng surname: Yu fullname: Yu, Chengpeng organization: Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Clinical Medicine Research Center for Hepatic Surgery of Hubei Province, Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, Hubei, 430030, People's Republic of China – sequence: 9 givenname: Hui-Fang surname: Liang fullname: Liang, Hui-Fang email: lianghuifang1997@126.com organization: Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Clinical Medicine Research Center for Hepatic Surgery of Hubei Province, Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, Hubei, 430030, People's Republic of China. lianghuifang1997@126.com – sequence: 10 givenname: Bixiang surname: Zhang fullname: Zhang, Bixiang email: bixiangzhang@163.com organization: Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Clinical Medicine Research Center for Hepatic Surgery of Hubei Province, Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, Hubei, 430030, People's Republic of China. bixiangzhang@163.com – sequence: 11 givenname: Xiaoping surname: Chen fullname: Chen, Xiaoping email: chenxpchenxp@163.com organization: Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Clinical Medicine Research Center for Hepatic Surgery of Hubei Province, Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, Hubei, 430030, People's Republic of China. chenxpchenxp@163.com |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30808376$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1128/MCB.18.1.629 10.1038/nrm3982 10.1128/MCB.05746-11 10.1038/nrc1934 10.1146/annurev.arplant.55.031903.141801 10.1158/0008-5472.CAN-16-2055 10.1038/onc.2011.443 10.18632/oncotarget.4082 10.1158/0008-5472.CAN-16-2098 10.1101/gad.1255304 10.1038/nrc2396 10.1128/MCB.18.1.546 10.1038/onc.2016.117 10.1158/0008-5472.CAN-17-3647 10.4161/cc.10.2.14530 10.1002/hep.26677 10.1016/j.molcel.2007.06.013 10.1038/nrc1881 10.1186/1478-811X-12-18 10.1002/cam4.1069 10.1073/pnas.1714938115 10.1101/gad.1676108 10.1038/ncomms10574 10.1074/jbc.M109.046789 10.1002/hep.22580 10.15252/embr.201438587 |
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Copyright | COPYRIGHT 2019 BioMed Central Ltd. Copyright © 2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. The Author(s). 2019 |
Copyright_xml | – notice: COPYRIGHT 2019 BioMed Central Ltd. – notice: Copyright © 2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: The Author(s). 2019 |
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DOI | 10.1186/s13046-019-1058-6 |
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References | A Ciechanover (1058_CR4) 2015; 16 JM Fraile (1058_CR22) 2012; 31 KI Nakayama (1058_CR5) 2006; 6 L Chen (1058_CR13) 2014; 12 J Jin (1058_CR7) 2004; 18 MK Tan (1058_CR9) 2011; 31 RN Aravalli (1058_CR2) 2008; 48 BH Yoo (1058_CR15) 2010; 285 1058_CR16 V Amador (1058_CR27) 2007; 27 J Ma (1058_CR6) 2017; 6 T Deng (1058_CR23) 2018; 115 T Abbas (1058_CR24) 2011; 10 T Abbas (1058_CR26) 2008; 22 R Sun (1058_CR11) 2018; 78 Y Johmura (1058_CR10) 2016; 7 WS El-Deiry (1058_CR19) 2016; 76 V Dulic (1058_CR25) 1998; 18 HT An (1058_CR12) 2016; 35 AB Niculescu 3rd (1058_CR20) 1998; 18 EM Kim (1058_CR18) 2017; 77 D Frescas (1058_CR21) 2008; 8 PA Farazi (1058_CR1) 2006; 6 J Smalle (1058_CR3) 2004; 55 J Kim (1058_CR17) 2014; 15 L Liu (1058_CR14) 2014; 59 X Tian (1058_CR8) 2015; 6 |
References_xml | – volume: 18 start-page: 629 year: 1998 ident: 1058_CR20 publication-title: Mol Cell Biol doi: 10.1128/MCB.18.1.629 contributor: fullname: AB Niculescu 3rd – volume: 16 start-page: 322 year: 2015 ident: 1058_CR4 publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm3982 contributor: fullname: A Ciechanover – volume: 31 start-page: 3687 year: 2011 ident: 1058_CR9 publication-title: Mol Cell Biol doi: 10.1128/MCB.05746-11 contributor: fullname: MK Tan – volume: 6 start-page: 674 year: 2006 ident: 1058_CR1 publication-title: Nat Rev Cancer doi: 10.1038/nrc1934 contributor: fullname: PA Farazi – volume: 55 start-page: 555 year: 2004 ident: 1058_CR3 publication-title: Annu Rev Plant Biol doi: 10.1146/annurev.arplant.55.031903.141801 contributor: fullname: J Smalle – volume: 76 start-page: 5189 year: 2016 ident: 1058_CR19 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-16-2055 contributor: fullname: WS El-Deiry – volume: 31 start-page: 2373 year: 2012 ident: 1058_CR22 publication-title: Oncogene doi: 10.1038/onc.2011.443 contributor: fullname: JM Fraile – volume: 6 start-page: 22767 year: 2015 ident: 1058_CR8 publication-title: Oncotarget doi: 10.18632/oncotarget.4082 contributor: fullname: X Tian – volume: 77 start-page: 3092 year: 2017 ident: 1058_CR18 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-16-2098 contributor: fullname: EM Kim – volume: 18 start-page: 2573 year: 2004 ident: 1058_CR7 publication-title: Genes Dev doi: 10.1101/gad.1255304 contributor: fullname: J Jin – volume: 8 start-page: 438 year: 2008 ident: 1058_CR21 publication-title: Nat Rev Cancer doi: 10.1038/nrc2396 contributor: fullname: D Frescas – volume: 18 start-page: 546 year: 1998 ident: 1058_CR25 publication-title: Mol Cell Biol doi: 10.1128/MCB.18.1.546 contributor: fullname: V Dulic – volume: 35 start-page: 5893 year: 2016 ident: 1058_CR12 publication-title: Oncogene doi: 10.1038/onc.2016.117 contributor: fullname: HT An – volume: 78 start-page: 5274 year: 2018 ident: 1058_CR11 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-17-3647 contributor: fullname: R Sun – volume: 10 start-page: 241 year: 2011 ident: 1058_CR24 publication-title: Cell Cycle doi: 10.4161/cc.10.2.14530 contributor: fullname: T Abbas – volume: 59 start-page: 531 year: 2014 ident: 1058_CR14 publication-title: Hepatology doi: 10.1002/hep.26677 contributor: fullname: L Liu – volume: 27 start-page: 462 year: 2007 ident: 1058_CR27 publication-title: Mol Cell doi: 10.1016/j.molcel.2007.06.013 contributor: fullname: V Amador – volume: 6 start-page: 369 year: 2006 ident: 1058_CR5 publication-title: Nat Rev Cancer doi: 10.1038/nrc1881 contributor: fullname: KI Nakayama – volume: 12 start-page: 18 year: 2014 ident: 1058_CR13 publication-title: Cell Commun Signal doi: 10.1186/1478-811X-12-18 contributor: fullname: L Chen – volume: 6 start-page: 1362 year: 2017 ident: 1058_CR6 publication-title: Cancer Med doi: 10.1002/cam4.1069 contributor: fullname: J Ma – volume: 115 start-page: 4678 year: 2018 ident: 1058_CR23 publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.1714938115 contributor: fullname: T Deng – volume: 22 start-page: 2496 year: 2008 ident: 1058_CR26 publication-title: Genes Dev doi: 10.1101/gad.1676108 contributor: fullname: T Abbas – volume: 7 year: 2016 ident: 1058_CR10 publication-title: Nat Commun doi: 10.1038/ncomms10574 contributor: fullname: Y Johmura – ident: 1058_CR16 – volume: 285 start-page: 5438 year: 2010 ident: 1058_CR15 publication-title: J Biol Chem doi: 10.1074/jbc.M109.046789 contributor: fullname: BH Yoo – volume: 48 start-page: 2047 year: 2008 ident: 1058_CR2 publication-title: Hepatology doi: 10.1002/hep.22580 contributor: fullname: RN Aravalli – volume: 15 start-page: 1062 year: 2014 ident: 1058_CR17 publication-title: EMBO Rep doi: 10.15252/embr.201438587 contributor: fullname: J Kim |
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Snippet | Deregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3 ligase, is a member of... Background Deregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3 ligase, is a... BACKGROUNDDeregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3 ligase, is a... Abstract Background Deregulation of ubiquitin ligases is related to the malignant progression of human cancers. F-box only protein 22 (FBXO22), an F-box E3... |
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SubjectTerms | Analysis Animal experimentation Breast cancer Cancer Carcinoma Cell cycle Cyclohexane Development and progression Experiments FBXO22 HCC Hepatocellular carcinoma Laboratory animals Ligases Liver Liver cancer Metastasis p21 Pathogenesis Phase transitions Proteins Signal transduction Tumorigenesis Tumors Ubiquitin Ubiquitination |
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Title | FBXO22 promotes the development of hepatocellular carcinoma by regulating the ubiquitination and degradation of p21 |
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