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4. Desmosomal COP9 regulates proteome degradation in arrhythmogenic right ventricular dysplasia/cardiomyopathy

Author

Liang, Yan, Lyon, Robert C, Pellman, Jason, Bradford, William H, Lange, Stephan, Bogomolovas, Julius, Dalton, Nancy D, Gu, Yusu, Bobar, Marcus, Lee, Mong-Hong, Iwakuma, Tomoo, Nigam, Vishal, Asimaki, Angeliki, Scheinman, Melvin, Peterson, Kirk L, and Sheikh, Farah

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Biotechnology, Heart Disease, Rare Diseases, Genetics, Cardiovascular, 2.1 Biological and endogenous factors, Adaptor Proteins, Signal Transducing, Animals, Arrhythmogenic Right Ventricular Dysplasia, COP9 Signalosome Complex, Desmosomes, Disease Models, Animal, Female, Humans, Male, Mice, Mice, Knockout, Proteolysis, Proteome, Cardiology, Muscle Biology, Ubiquitin-proteosome system, Medical and Health Sciences, Immunology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Dysregulated protein degradative pathways are increasingly recognized as mediators of human disease. This mechanism may have particular relevance to desmosomal proteins that play critical structural roles in both tissue architecture and cell-cell communication, as destabilization/breakdown of the desmosomal proteome is a hallmark of genetic-based desmosomal-targeted diseases, such as the cardiac disease arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). However, no information exists on whether there are resident proteins that regulate desmosomal proteome homeostasis. Here, we uncovered a cardiac constitutive photomorphogenesis 9 (COP9) desmosomal resident protein complex, composed of subunit 6 of the COP9 signalosome (CSN6), that enzymatically restricted neddylation and targeted desmosomal proteome degradation. CSN6 binding, localization, levels, and function were affected in hearts of classic mouse and human models of ARVD/C affected by desmosomal loss and mutations, respectively. Loss of desmosomal proteome degradation control due to junctional reduction/loss of CSN6 and human desmosomal mutations destabilizing junctional CSN6 were also sufficient to trigger ARVD/C in mice. We identified a desmosomal resident regulatory complex that restricted desmosomal proteome degradation and disease.

Published
2021

10. CSN6‐SPOP‐HMGCS1 Axis Promotes Hepatocellular Carcinoma Progression via YAP1 Activation

Author

Li, Kai, primary, Zhang, Jiayu, additional, Lyu, Haiwen, additional, Yang, Jinneng, additional, Wei, Wenxia, additional, Wang, Yuzhi, additional, Luo, Haidan, additional, Zhang, Yijing, additional, Jiang, Xin, additional, Yi, Hairong, additional, Wang, Mengan, additional, Zhang, Caiyun, additional, Wu, Kang, additional, Xiao, Lishi, additional, Wen, Weijie, additional, Xu, Hui, additional, Li, Guolin, additional, Wan, Yunle, additional, Yang, Fang, additional, Yang, Runxiang, additional, Fu, Xinhui, additional, Qin, Baifu, additional, Zhou, Zhongguo, additional, Zhang, Haipeng, additional, and Lee, Mong‐Hong, additional

Published
2024
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11. Obesity-associated NLRC4 inflammasome activation drives breast cancer progression.

Author

Kolb, Ryan, Phan, Liem, Borcherding, Nicholas, Liu, Yinghong, Yuan, Fang, Janowski, Ann M, Xie, Qing, Markan, Kathleen R, Li, Wei, Potthoff, Matthew J, Fuentes-Mattei, Enrique, Ellies, Lesley G, Knudson, C Michael, Lee, Mong-Hong, Yeung, Sai-Ching J, Cassel, Suzanne L, Sutterwala, Fayyaz S, and Zhang, Weizhou

Subjects
Breast, Lymphocytes, Tumor-Infiltrating, Cell Line, Tumor, Myeloid Cells, Animals, Mice, Inbred C57BL, Humans, Mice, Breast Neoplasms, Mammary Neoplasms, Experimental, Obesity, Disease Progression, Vascular Endothelial Growth Factor A, Calcium-Binding Proteins, Neoplasm Transplantation, Signal Transduction, Female, Apoptosis Regulatory Proteins, Interleukin-1beta, CARD Signaling Adaptor Proteins, Inflammasomes, Breast Cancer, Nutrition, Cancer, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Cardiovascular, Lymphocytes, Tumor-Infiltrating, Cell Line, Tumor, Inbred C57BL, Mammary Neoplasms, Experimental
Abstract

Obesity is associated with an increased risk of developing breast cancer and is also associated with worse clinical prognosis. The mechanistic link between obesity and breast cancer progression remains unclear, and there has been no development of specific treatments to improve the outcome of obese cancer patients. Here we show that obesity-associated NLRC4 inflammasome activation/ interleukin (IL)-1 signalling promotes breast cancer progression. The tumour microenvironment in the context of obesity induces an increase in tumour-infiltrating myeloid cells with an activated NLRC4 inflammasome that in turn activates IL-1β, which drives disease progression through adipocyte-mediated vascular endothelial growth factor A (VEGFA) expression and angiogenesis. Further studies show that treatment of mice with metformin inhibits obesity-associated tumour progression associated with a marked decrease in angiogenesis. This report provides a causal mechanism by which obesity promotes breast cancer progression and lays out a foundation to block NLRC4 inflammasome activation or IL-1β signalling transduction that may be useful for the treatment of obese cancer patients.

Published
2016

15. eIF3f Mediates SGOC Pathway Reprogramming by Enhancing Deubiquitinating Activity in Colorectal Cancer

Author

Pan, Qihao, primary, Yu, Fenghai, additional, Jin, Huilin, additional, Zhang, Peng, additional, Huang, Xiaoling, additional, Peng, Jingxuan, additional, Xie, Xiaoshan, additional, Li, Xiangli, additional, Ma, Ning, additional, Wei, Yue, additional, Wen, Weijie, additional, Zhang, Jieping, additional, Zhang, Boyu, additional, Yu, Hongyan, additional, Xiao, Yuanxun, additional, Liu, Ran‐yi, additional, Liu, Qingxin, additional, Meng, Xiangqi, additional, and Lee, Mong‐Hong, additional

Published
2023
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21. Supplementary Video from Kinetic Modeling and Constrained Reconstruction of Hyperpolarized [1-13C]-Pyruvate Offers Improved Metabolic Imaging of Tumors

Author

Bankson, James A., primary, Walker, Christopher M., primary, Ramirez, Marc S., primary, Stefan, Wolfgang, primary, Fuentes, David, primary, Merritt, Matthew E., primary, Lee, Jaehyuk, primary, Sandulache, Vlad C., primary, Chen, Yunyun, primary, Phan, Liem, primary, Chou, Ping-Chieh, primary, Rao, Arvind, primary, Yeung, Sai-Ching J., primary, Lee, Mong-Hong, primary, Schellingerhout, Dawid, primary, Conrad, Charles A., primary, Malloy, Craig, primary, Sherry, A. Dean, primary, Lai, Stephen Y., primary, and Hazle, John D., primary

Published
2023
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22. Supplementary Table from Kinetic Modeling and Constrained Reconstruction of Hyperpolarized [1-13C]-Pyruvate Offers Improved Metabolic Imaging of Tumors

Author

Bankson, James A., primary, Walker, Christopher M., primary, Ramirez, Marc S., primary, Stefan, Wolfgang, primary, Fuentes, David, primary, Merritt, Matthew E., primary, Lee, Jaehyuk, primary, Sandulache, Vlad C., primary, Chen, Yunyun, primary, Phan, Liem, primary, Chou, Ping-Chieh, primary, Rao, Arvind, primary, Yeung, Sai-Ching J., primary, Lee, Mong-Hong, primary, Schellingerhout, Dawid, primary, Conrad, Charles A., primary, Malloy, Craig, primary, Sherry, A. Dean, primary, Lai, Stephen Y., primary, and Hazle, John D., primary

Published
2023
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23. Data from Kinetic Modeling and Constrained Reconstruction of Hyperpolarized [1-13C]-Pyruvate Offers Improved Metabolic Imaging of Tumors

Author

Bankson, James A., primary, Walker, Christopher M., primary, Ramirez, Marc S., primary, Stefan, Wolfgang, primary, Fuentes, David, primary, Merritt, Matthew E., primary, Lee, Jaehyuk, primary, Sandulache, Vlad C., primary, Chen, Yunyun, primary, Phan, Liem, primary, Chou, Ping-Chieh, primary, Rao, Arvind, primary, Yeung, Sai-Ching J., primary, Lee, Mong-Hong, primary, Schellingerhout, Dawid, primary, Conrad, Charles A., primary, Malloy, Craig, primary, Sherry, A. Dean, primary, Lai, Stephen Y., primary, and Hazle, John D., primary

Published
2023
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24. Supplementary Data from CSN6 Mediates Nucleotide Metabolism to Promote Tumor Development and Chemoresistance in Colorectal Cancer

Author

Zou, Shaomin, primary, Qin, Baifu, primary, Yang, Ziqing, primary, Wang, Wencong, primary, Zhang, Jieping, primary, Zhang, Yijing, primary, Meng, Manqi, primary, Feng, Junyan, primary, Xie, Yunling, primary, Fang, Ling, primary, Xiao, Lishi, primary, Zhang, Peng, primary, Meng, Xiangqi, primary, Choi, Hyun Ho, primary, Wen, Weijie, primary, Pan, Qihao, primary, Ghesquière, Bart, primary, Lan, Ping, primary, Lee, Mong-Hong, primary, and Fang, Lekun, primary

Published
2023
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25. Supplementary Table Legend from Hepatocyte Growth Factor/cMET Pathway Activation Enhances Cancer Hallmarks in Adrenocortical Carcinoma

Author

Phan, Liem M., primary, Fuentes-Mattei, Enrique, primary, Wu, Weixin, primary, Velazquez-Torres, Guermarie, primary, Sircar, Kanishka, primary, Wood, Christopher G., primary, Hai, Tao, primary, Jimenez, Camilo, primary, Cote, Gilbert J., primary, Ozsari, Levent, primary, Hofmann, Marie-Claude, primary, Zheng, Siyuan, primary, Verhaak, Roeland, primary, Pagliaro, Lance, primary, Cortez, Maria Angelica, primary, Lee, Mong-Hong, primary, Yeung, Sai-Ching J., primary, and Habra, Mouhammed Amir, primary

Published
2023
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27. Data from Hepatocyte Growth Factor/cMET Pathway Activation Enhances Cancer Hallmarks in Adrenocortical Carcinoma

Author

Phan, Liem M., primary, Fuentes-Mattei, Enrique, primary, Wu, Weixin, primary, Velazquez-Torres, Guermarie, primary, Sircar, Kanishka, primary, Wood, Christopher G., primary, Hai, Tao, primary, Jimenez, Camilo, primary, Cote, Gilbert J., primary, Ozsari, Levent, primary, Hofmann, Marie-Claude, primary, Zheng, Siyuan, primary, Verhaak, Roeland, primary, Pagliaro, Lance, primary, Cortez, Maria Angelica, primary, Lee, Mong-Hong, primary, Yeung, Sai-Ching J., primary, and Habra, Mouhammed Amir, primary

Published
2023
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29. Supplementary Tables S1-S12 from Hepatocyte Growth Factor/cMET Pathway Activation Enhances Cancer Hallmarks in Adrenocortical Carcinoma

Author

Phan, Liem M., primary, Fuentes-Mattei, Enrique, primary, Wu, Weixin, primary, Velazquez-Torres, Guermarie, primary, Sircar, Kanishka, primary, Wood, Christopher G., primary, Hai, Tao, primary, Jimenez, Camilo, primary, Cote, Gilbert J., primary, Ozsari, Levent, primary, Hofmann, Marie-Claude, primary, Zheng, Siyuan, primary, Verhaak, Roeland, primary, Pagliaro, Lance, primary, Cortez, Maria Angelica, primary, Lee, Mong-Hong, primary, Yeung, Sai-Ching J., primary, and Habra, Mouhammed Amir, primary

Published
2023
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30. Supplementary Figures S1-S6 from Hepatocyte Growth Factor/cMET Pathway Activation Enhances Cancer Hallmarks in Adrenocortical Carcinoma

Author

Phan, Liem M., primary, Fuentes-Mattei, Enrique, primary, Wu, Weixin, primary, Velazquez-Torres, Guermarie, primary, Sircar, Kanishka, primary, Wood, Christopher G., primary, Hai, Tao, primary, Jimenez, Camilo, primary, Cote, Gilbert J., primary, Ozsari, Levent, primary, Hofmann, Marie-Claude, primary, Zheng, Siyuan, primary, Verhaak, Roeland, primary, Pagliaro, Lance, primary, Cortez, Maria Angelica, primary, Lee, Mong-Hong, primary, Yeung, Sai-Ching J., primary, and Habra, Mouhammed Amir, primary

Published
2023
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35. CSN6 Mediates Nucleotide Metabolism to Promote Tumor Development and Chemoresistance in Colorectal Cancer

Author

Zou, Shaomin, primary, Qin, Baifu, additional, Yang, Ziqing, additional, Wang, Wencong, additional, Zhang, Jieping, additional, Zhang, Yijing, additional, Meng, Manqi, additional, Feng, Junyan, additional, Xie, Yunling, additional, Fang, Ling, additional, Xiao, Lishi, additional, Zhang, Peng, additional, Meng, Xiangqi, additional, Choi, Hyun Ho, additional, Wen, Weijie, additional, Pan, Qihao, additional, Ghesquière, Bart, additional, Lan, Ping, additional, Lee, Mong-Hong, additional, and Fang, Lekun, additional

Published
2022
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41. Aurora B kinase phosphorylates and instigates degradation of p53

Author

Gully, Chris P., Velazquez-Torres, Guermarie, Shin, Ji-Hyun, Fuentes-Mattei, Enrique, Wang, Edward, Carlock, Colin, Chen, Jian, Rothenberg, Daniel, Adams, Henry P., Choi, Hyun Ho, Guma, Sergei, Phan, Liem, Chou, Ping-Chieh, Su, Chun-Hui, Zhang, Fanmao, Chen, Jiun-Sheng, Yang, Tsung-Ying, Yeung, Sai-Ching J., and Lee, Mong-Hong

Published
2012

46. Abstract MP218: Cop9 Signalosome Subunit 6 Restricts Desmosomal Proteome Degradation To Prevent Desmosomal Targeted Cardiac Disease

Author

Liang, Yan, primary, Lyon, Robert, additional, Pellman, Jason, additional, Bradford, William, additional, Lange, Stephan, additional, Bogomolovas, Julijus, additional, Dalton, Nancy, additional, Gu, Yusu, additional, Bobar, Marcus, additional, Lee, Mong-Hong, additional, Iwakuma, Tomoo, additional, Nigam, Vishal, additional, Asimaki, Angeliki, additional, Scheinman, Melvin, additional, Peterson, Kirk L, additional, and Sheikh, Farah, additional

Published
2021
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49. Subunit 6 of the COP9 signalosome promotes tumorigenesis in mice through stabilization of MDM2 and is upregulated in human cancers

Author

Zhao, Ruiying, Yeung, Sai-Ching J., Chen, Jian, Iwakuma, Tomoo, Su, Chun-Hui, Chen, Bo, Qu, Changju, Zhang, Fanmao, Chen, You-Tzung, Lin, Yu-Li, Lee, Dung-Fang, Jin, Feng, Zhu, Rui, Shaikenov, Tattym, Sarbassov, Dos, Sahin, Aysegul, Wang, Huamin, Wang, Hua, Lai, Chien-Chen, Tsai, Fuu-Jen, Lozano, Guillermina, and Lee, Mong-Hong

Subjects
Plants -- Photomorphogenesis, Tumor suppressor genes -- Physiological aspects -- Research -- Genetic aspects, DNA damage -- Research -- Physiological aspects -- Genetic aspects, Breast cancer -- Risk factors -- Genetic aspects -- Research, Health care industry
Abstract

The mammalian constitutive photomorphogenesis 9 (COP9) signalosome (CSN), a protein complex involved in embryonic development, is implicated in cell cycle regulation and the DNA damage response. Its role in tumor development, however, remains unclear. Here, we have shown that the COP9 subunit 6 (CSN6) gene is amplified in human breast cancer specimens, and the CSN6 protein is upregulated in human breast and thyroid tumors. CSN6 expression positively correlated with expression of murine double minute 2 (MDM2), a potent negative regulator of the p53 tumor suppressor. Expression of CSN6 appeared to prevent MDM2 autoubiquitination at lysine 364, resulting in stabilization of MDM2 and degradation of p53. Mice in which Csn6 was deleted died early in embryogenesis (E7.5). Embryos lacking both Csn6 and p53 survived to later in embryonic development (E10.5), which suggests that loss of p53 could partially rescue the effect of loss of Csn6. Mice heterozygous for Csn6 were sensitized to γ-irradiation--induced, p53-dependent apoptosis in both the thymus and the developing CNS. These mice were also less susceptible than wild-type mice to γ-irradiation--induced tumorigenesis. These results suggest that loss of CSN6 enhances p53-mediated tumor suppression in vivo and that CSN6 plays an important role in regulating DNA damage--associated apoptosis and tumorigenesis through control of the MDM2-p53 signaling pathway., Introduction The constitutive photomorphogenesis 9 (COP9) signalosome (CSN) was originally identified from Arabidopsis mutants that mimic light-induced seedling development when grown in the dark (1). The mammalian COP9 contains 8 [...]

Published
2011
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50. Effects of Obesity on Transcriptomic Changes and Cancer Hallmarks in Estrogen Receptor-Positive Breast Cancer

Author

Fuentes-Mattei, Enrique, Velazquez-Torres, Guermarie, Phan, Liem, Zhang, Fanmao, Chou, Ping-Chieh, Shin, Ji-Hyun, Choi, Hyun Ho, Chen, Jiun-Sheng, Zhao, Ruiying, Chen, Jian, Gully, Chris, Carlock, Colin, Qi, Yuan, Zhang, Ya, Wu, Yun, Esteva, Francisco J., Luo, Yongde, McKeehan, Wallace L., Ensor, Joe, Hortobagyi, Gabriel N., Pusztai, Lajos, Symmans, Fraser W., Lee, Mong-Hong, and Yeung, Sai-Ching Jim

Published
2014
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