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      RNF6 promotes the migration and invasion of breast cancer by promoting the ubiquitination and degradation of MST1

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          Abstract

          Ring finger protein 6 ( RNF6), a member of E3 ubiquitin ligases, plays a potential role as a tumour promoter in numerous carcinomas. However, the role and expression of RNF6 in breast cancer (BC) remains to be elucidated. The present study showed that RNF6 upregulation was detected in BC tissues and was associated with short survival in patients with BC. Multivariate analysis also revealed that RNF6 overexpression is an independent predictor for poor outcome of patients with BC. Furthermore, migration and metastasis assay indicated that RNF6 silencing significantly inhibited the invasion and migration of BC cells in vivo and in vitro, and RNF6 suppression decreased YES-associated protein (YAP) expression. RNF6 promoted the metastatic ability of BC cells via YAP. Mechanistically, RNF6 interacts with mammalian STE20-like protein kinase 1 (MST1), a key factor that regulates YAP, and promoted its ubiquitination and degradation. Additionally, RNF6 regulated YAP signalling by promoting ubiquitination and degradation of MST1 in BC. Taken together, these data may highlight a role of RNF6 in BC, which could serve as a valuable prognostic indicator and potential therapeutic target for patients with BC.

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          Cancer statistics, 2018

          Kimberly D Miller, Rebecca Siegel, Ahmedin Jemal (2018)
          Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the United States and compiles the most recent data on cancer incidence, mortality, and survival. Incidence data, available through 2014, were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data, available through 2015, were collected by the National Center for Health Statistics. In 2018, 1,735,350 new cancer cases and 609,640 cancer deaths are projected to occur in the United States. Over the past decade of data, the cancer incidence rate (2005-2014) was stable in women and declined by approximately 2% annually in men, while the cancer death rate (2006-2015) declined by about 1.5% annually in both men and women. The combined cancer death rate dropped continuously from 1991 to 2015 by a total of 26%, translating to approximately 2,378,600 fewer cancer deaths than would have been expected if death rates had remained at their peak. Of the 10 leading causes of death, only cancer declined from 2014 to 2015. In 2015, the cancer death rate was 14% higher in non-Hispanic blacks (NHBs) than non-Hispanic whites (NHWs) overall (death rate ratio [DRR], 1.14; 95% confidence interval [95% CI], 1.13-1.15), but the racial disparity was much larger for individuals aged <65 years (DRR, 1.31; 95% CI, 1.29-1.32) compared with those aged ≥65 years (DRR, 1.07; 95% CI, 1.06-1.09) and varied substantially by state. For example, the cancer death rate was lower in NHBs than NHWs in Massachusetts for all ages and in New York for individuals aged ≥65 years, whereas for those aged <65 years, it was 3 times higher in NHBs in the District of Columbia (DRR, 2.89; 95% CI, 2.16-3.91) and about 50% higher in Wisconsin (DRR, 1.78; 95% CI, 1.56-2.02), Kansas (DRR, 1.51; 95% CI, 1.25-1.81), Louisiana (DRR, 1.49; 95% CI, 1.38-1.60), Illinois (DRR, 1.48; 95% CI, 1.39-1.57), and California (DRR, 1.45; 95% CI, 1.38-1.54). Larger racial inequalities in young and middle-aged adults probably partly reflect less access to high-quality health care. CA Cancer J Clin 2018;68:7-30. © 2018 American Cancer Society.
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            Intercellular interaction dictates cancer cell ferroptosis via Merlin-YAP signalling

            Jiao Wu, Alexander Minikes, Minghui Gao … (2019)
            SUMMARY Ferroptosis, a cell death process driven by cellular metabolism and iron-dependent lipid peroxidation, is implicated in various diseases such as ischemic organ damage and cancer 1,2 . As a central regulator of ferroptosis, the enzyme glutathione peroxidase 4 (GPX4) protects cells from ferroptosis by neutralizing lipid peroxides, which are byproducts of cellular metabolism; as such, inhibiting GPX4 directly, or indirectly by depriving its substrate glutathione or building blocks of glutathione (such as cysteine), can trigger ferroptosis 3 . Ferroptosis contributes to the antitumour function of multiple tumour suppressors including p53, BAP1, and fumarase 4-7 . Counterintuitively, mesenchymal cancer cells, which are prone to metastasis and often resistant to various treatments, have shown to be highly susceptible to ferroptosis 8,9 . Here, we demonstrate that ferroptosis can be regulated non-cell autonomously by cadherin-mediated intercellular contacts. In epithelial cells, E-cadherin-mediated intercellular interaction suppresses ferroptosis through intracellular Merlin-Hippo signalling. Antagonizing this signalling axis unleashes the activity of the proto-oncogenic transcriptional co-activator YAP to promote ferroptosis through upregulation of multiple ferroptosis modulators, including acyl-CoA synthetase long chain family member 4 (ACSL4) and transferrin receptor. This finding provides mechanistic insights into the observations that epithelial mesenchymal transition (EMT)/metastasis-prone cancer cells are highly sensitive to ferroptosis 8 . Importantly, the regulation of ferroptosis by cell-cell contact and Merlin-YAP signalling is not limited to epithelial cells; a similar mechanism also modulates ferroptosis in some non-epithelial cells. Finally, we found that genetic inactivation of the tumour suppressor Merlin, a frequent tumourigenic event in mesothelioma 10,11 , renders cancer cells more sensitive to ferroptosis in an orthotopic mouse model of malignant mesothelioma. Together, this study unveils the role of intercellular interaction and intracellular Merlin-YAP signalling in dictating ferroptotic death; it also suggests that malignant mutations in Merlin-YAP signalling can serve as biomarkers predicting cancer cell responsiveness to future ferroptosis-inducing therapies.
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              RINGs of good and evil: RING finger ubiquitin ligases at the crossroads of tumour suppression and oncogenesis.

              Stanley Lipkowitz, Allan M. Weissman (2011)
              The ubiquitin-proteasome system has numerous crucial roles in physiology and pathophysiology. Fundamental to the specificity of this system are ubiquitin-protein ligases (E3s). Of these, the majority are RING finger and RING finger-related E3s. Many RING finger E3s have roles in processes that are central to the maintenance of genomic integrity and cellular homeostasis, such as the anaphase promoting complex/cyclosome (APC/C), the SKP1-cullin 1-F-box protein (SCF) E3s, MDM2, BRCA1, Fanconi anaemia proteins, CBL proteins, von Hippel-Lindau tumour suppressor (VHL) and SIAH proteins. As a result, many RING finger E3s are implicated in either the suppression or the progression of cancer. This Review summarizes current knowledge in this area.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Exp Ther Med
                Journal ID (iso-abbrev): Exp Ther Med
                Journal ID (publisher-id): ETM
                Title: Experimental and Therapeutic Medicine
                Publisher: D.A. Spandidos
                ISSN (Print): 1792-0981
                ISSN (Electronic): 1792-1015
                Publication date (Print): February 2022
                Publication date (Electronic): 06 December 2021
                Publication date PMC-release: 06 December 2021
                Volume: 23
                Issue: 2
                Electronic Location Identifier: 118
                Affiliations
                [1 ]Department of General Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330009, P.R. China
                [2 ]Department of Breast Surgery, The Third Hospital of Nanchang, Nanchang, Jiangxi 330006, P.R. China
                [3 ]Jiangxi Provincial Key Laboratory for Breast Diseases, The Third Hospital of Nanchang, Nanchang, Jiangxi 330006, P.R. China
                Author notes
                Correspondence to: Professor Zhigang Jie, Department of General Surgery, The First Affiliated Hospital of Nanchang University, 17 Yongwai Street, Nanchang, Jiangxi 330009, P.R. China zhigangjie1963@ 123456126.com
                Article
                Publisher ID: ETM-0-0-11041
                DOI: 10.3892/etm.2021.11041
                PMC ID: 8713179
                SO-VID: 14f178fe-c303-4f92-a879-edd69b18c953
                Copyright © Copyright: © Huang et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 06 November 2019
                Date accepted : 26 August 2020
                Funding
                Funding: This study was supported by a grant from the National Natural Science Foundation of China (grant no. 81960503).
                Categories
                Subject: Articles

                ScienceOpen disciplines: Medicine
                Keywords: ring finger protein 6,breast cancer,mammalian ste20-like protein kinase,migration and invasion,ubiquitination,degradation
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: ring finger protein 6, breast cancer, mammalian ste20-like protein kinase, migration and invasion, ubiquitination, degradation

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