Cullin 3 targets methionine adenosyltransferase IIα for ubiquitylation‐mediated degradation and regulates colorectal cancer cell proliferation

Wang, Jian; Zhu, Zhiliang; Yang, Hong-Chang; Zhang, Ye; Zhao, Xiangmo; Zhang, Min; Liu, Yingbin; Xu, Yingying; Lei, Qun-Ying

doi:10.1111/febs.13759

Cited by 17 publications

(16 citation statements)

References 49 publications

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“… 17,18 Cullin 3 (Cul3), a scaffold protein involved in the degradation of a variety of intracellular proteins, is a major regulator of the cell cycle and developmental processes. 19,20 The N‐terminal BTB domains of some KCTD proteins can be used as bridges connecting Cul3 and substrates and play the role of Cul3 ubiquitin ligase. They have multiple biological functions and are closely related to protein ubiquitination 21,22 .…”

Section: Introductionmentioning

confidence: 99%

KCTD11 inhibits progression of lung cancer by binding to β‐catenin to regulate the activity of the Wnt and Hippo pathways

Yang

Han

et al. 2021

J Cellular Molecular Medi

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KCTD11 has been reported to be a potential tumour suppressor in several tumour types. However, the expression of KCTD11 and its role has not been reported in human non‐small cell lung cancer (NSCLC). Whether its potential molecular mechanism is related to its BTB domain is also unknown. The expression of KCTD11 in 139 NSCLC tissue samples was detected by immunohistochemistry, and its correlation with clinicopathological factors was analysed. The effect of KCTD11 on the biological behaviour of lung cancer cells was verified in vitro and in vivo. Its effect on the epithelial‐mesenchymal transition(EMT)process and the Wnt/β‐catenin and Hippo/YAP pathways were observed by Western blot, dual‐luciferase assay, RT‐qPCR, immunofluorescence and immunoprecipitation. KCTD11 is under‐expressed in lung cancer tissues and cells and was negatively correlated with the degree of differentiation, tumour‐node‐metastasis (TNM) stage and lymph node metastasis. Low KCTD11 expression was associated with poor prognosis. KCTD11 overexpression inhibited the proliferation and migration of lung cancer cells. Further studies indicated that KCTD11 inhibited the Wnt pathway, activated the Hippo pathway and inhibited EMT processes by inhibiting the nuclear translocation of β‐catenin and YAP. KCTD11 lost its stimulatory effect on the Hippo pathway after knock down of β‐catenin. These findings confirm that KCTD11 inhibits β‐catenin and YAP nuclear translocation as well as the malignant phenotype of lung cancer cells by interacting with β‐catenin. This provides an important experimental basis for the interaction between KCTD11, β‐catenin and YAP, further revealing the link between the Wnt and Hippo pathways.

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Section: Introductionmentioning

confidence: 99%

KCTD11 inhibits progression of lung cancer by binding to β‐catenin to regulate the activity of the Wnt and Hippo pathways

Yang

Han

et al. 2021

J Cellular Molecular Medi

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“…Cullin 3 (CUL3) is the core component of multiple cullin-RING-based BCR (BTB-CUL3-RBX1) E3 ubiquitin-protein ligase complexes, which mediate the ubiquitination and subsequent proteasomal degradation of target proteins. As shown by Wang, CUL3 downregulation rescues folate deprivation-induced MAT II α exhaustion and growth arrest in CRC cells [37].…”

Section: Discussionmentioning

confidence: 99%

Ranking Cancer Proteins by Integrating PPI Network and Protein Expression Profiles

Ren

Shang

Wang

et al. 2019

BioMed Research International

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Proteomics, the large-scale analysis of proteins, is contributing greatly to understanding gene function in the postgenomic era. However, disease protein ranking using shotgun proteomics data has not been fully evaluated. In this study, we prioritized disease-related proteins by integrating the protein-protein interaction (PPI) network and protein differential expression profiles from colon and rectal cancer (CRC) or breast cancer (BC) proteomics. We applied Local Ranking (LR) and Global Ranking (GR) methods in network with three kinds of protein sets as a priori knowledge, which were known disease proteins (KDPs) that were collected from the Online Mendelian Inheritance in Man (OMIM) database, differentially expressed proteins (DEPs), and the collection of KDPs and their direct neighborhood with differential expression (eKDPs). The cross-validations showed that GR method outperformed LR method while using eKDPs as the initial training showed significantly higher accuracy compared to using the other two a priori sets. And then we validated the top ranked proteins using RNAi-based loss-of-function screens in the DepMap database. The results showed that 75% of top 20 proteins in CRC are necessary for tumor survival. In summary, the network-based Global Ranking with protein differential expression can efficiently prioritize cancer-related proteins and discover new candidate cancer genes or proteins.

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“…Although the role of MAT is most well studied in liver cancer, there is continuously emerging evidence of MAT2A or MAT2B dysregulation in other cancers, including T cell leukemia ( Jani et al 2009) and colon carcinoma (Chen et al 2007, Wang et al 2016, as well as gastric (T. , breast (Phuong et al 2016), pancreatic, and prostate cancer (Tomasi et al 2017) (reviewed in Maldonado et al 2018). Furthermore, two recent studies have suggested a role for SAM biosynthesis in cancer stem cell biology.…”

Section: Mat2a and Its Role In Cancermentioning

confidence: 99%

Cancer Dependencies: PRMT5 and MAT2A in MTAP/p16-Deleted Cancers

Marjon

Kalev

Marks

2021

Annu. Rev. Cancer Biol.

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Discovery of targeted therapies that selectively exploit the genetic inactivation of specific tumor suppressors remains a major challenge. This includes the prevalent deletion of the CDKN2A/ MTAP locus, which was first reported nearly 40 years ago. The more recent advent of RNA interference and functional genomic screening technologies led to the identification of hidden collateral lethalities occurring with passenger deletions of MTAP in cancer cells. In particular, small-molecule inhibition of the type II arginine methyltransferase PRMT5 and the S-adenosylmethionine-producing enzyme MAT2A each presents a precision medicine approach for the treatment of patients whose tumors have homozygous loss of MTAP. In this review, we highlight key aspects of MTAP, PRMT5, and MAT2A biology to provide a conceptual framework for developing novel therapeutic strategies in tumors with MTAP deletion and to summarize ongoing efforts to drug PRMT5 and MAT2A. Expected final online publication date for the Annual Review of Cancer Biology, Volume 5 is March 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

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Cullin 3 targets methionine adenosyltransferase IIα for ubiquitylation‐mediated degradation and regulates colorectal cancer cell proliferation

Cited by 17 publications

References 49 publications

KCTD11 inhibits progression of lung cancer by binding to β‐catenin to regulate the activity of the Wnt and Hippo pathways

KCTD11 inhibits progression of lung cancer by binding to β‐catenin to regulate the activity of the Wnt and Hippo pathways

Ranking Cancer Proteins by Integrating PPI Network and Protein Expression Profiles

Cancer Dependencies: PRMT5 and MAT2A in MTAP/p16-Deleted Cancers

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