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      Transforming Stimulated Clone 22 (TSC-22) Interacts Directly with Bromodomain-Containing Protein 7 (BRD7) to Enhance the Inhibition of Extracellular Signal-Regulate Kinase (ERK) Pathway in Ovarian Cancer

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          Abstract

          Bromodomain-containing protein 7 (BRD7) participates in many cellular processes and embryo development. BRD7 is down-regulated in various cancers and evidence of its tumor suppressor function has been accumulating. Here, we identified transforming stimulated clone 22 (TSC-22) as a novel BRD7 interacting protein and show its novel function as a positive regulator of BRD7. We found that TSC-22 expression potentiated the inactivation of the extracellular signal-regulate kinase (ERK) pathway by BRD7. Our data establishes TSC-22 as a modulator of BRD7 and unravels the molecular mechanisms that drive the synergistic tumor-suppressing effects of TSC-22 and BRD7. Our findings may open new avenues for developing novel molecular therapies for tumors exhibiting down-regulated BRD7 and/or TSC-22.

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          The landscape of somatic copy-number alteration across human cancers

          Rameen Beroukhim, Craig H. Mermel, Dale Porter … (2010)
          A powerful way to discover key genes playing causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. Here, we report high-resolution analyses of somatic copy-number alterations (SCNAs) from 3131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across multiple cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several gene families are enriched among these regions of focal SCNA, including the BCL2 family of apoptosis regulators and the NF-κB pathway. We show that cancer cells harboring amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend upon expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in multiple cancer types.
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            WNT signalling pathways as therapeutic targets in cancer.

            Jamie N Anastas, Randall T Moon (2013)
            Since the initial discovery of the oncogenic activity of WNT1 in mouse mammary glands, our appreciation for the complex roles for WNT signalling pathways in cancer has increased dramatically. WNTs and their downstream effectors regulate various processes that are important for cancer progression, including tumour initiation, tumour growth, cell senescence, cell death, differentiation and metastasis. Although WNT signalling pathways have been difficult to target, improved drug-discovery platforms and new technologies have facilitated the discovery of agents that can alter WNT signalling in preclinical models, thus setting the stage for clinical trials in humans.
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              The regulation of β-catenin activity and function in cancer: therapeutic opportunities

              Shuang Shang, Fang Hua, Zhuo-Wei Hu (2017)
              Wnt/β-catenin signaling is an evolutionarily conserved and versatile pathway that is known to be involved in embryonic development, tissue homeostasis and a wide variety of human diseases. Aberrant activation of this pathway gives rise to the accumulation of β-catenin in the nucleus and promotes the transcription of many oncogenes such as c-Myc and CyclinD-1. As a result, it contributes to carcinogenesis and tumor progression of several cancers, including colon cancer, hepatocellular carcinoma, pancreatic cancer, lung cancer and ovarian cancer. β-Catenin is a pivotal component of the Wnt signaling pathway and it is tightly regulated at three hierarchical levels: protein stability, subcellular localization and transcriptional activity. Uncovering the regulatory mechanisms of β-catenin will provide new insights into the pathogenesis of cancer and other diseases, as well as new therapeutic strategies against these diseases. In this review we dissect the concrete regulatory mechanisms of β-catenin from three aspects mentioned above. Then we focus on the role of β-catenin in cancer initiation, progression, dormancy, immunity and cancer stem cell maintenance. At last, we summarize the recent progress in the development of agents for the pharmacological modulation of β-catenin activity in cancer therapy.
              Article 0 comments Cited 255 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Dev Reprod
                Journal ID (iso-abbrev): Dev Reprod
                Journal ID (publisher-id): Dev. Reprod.
                Journal ID (publisher-id): dr
                Title: Development & Reproduction
                Publisher: Korean Society of Developmental Biology
                ISSN (Print): 2465-9525
                ISSN (Electronic): 2465-9541
                Publication date (Print): September 2022
                Publication date (Electronic): 30 September 2022
                Volume: 26
                Issue: 3
                Pages: 117-126
                Affiliations
                [1 ]Department of Life Science, YongIn University , Yongin 17092, Korea
                Author notes
                [† ] Corresponding author Seung-Hoon Lee, Department of Life Science, YongIn University, Yongin 17092, Korea. Tel: +82-31-8020-2780, E-mail: shlee@ 123456yongin.ac.kr
                Author information
                https://orcid.org/0000-0001-9409-1422
                https://orcid.org/0000-0002-5170-090X
                Article
                Publisher ID: dr-26-3-117
                DOI: 10.12717/DR.2022.26.3.117
                PMC ID: 9578317
                PubMed ID: 36285148
                SO-VID: 7cc86abe-b64f-4e50-8d77-08213d8aa6f0
                Copyright © © Copyright 2022 The Korean Society of Developmental Biology
                License:

                This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creative-commons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 03 June 2022
                Date revision received : 08 August 2022
                Date accepted : 02 September 2022
                Funding
                Funded by: CrossRef http://dx.doi.org/10.13039/501100002615, Yong In University;
                Categories
                Subject: Review
                Custom metadata
                crossmark 2022-09-30

                Keywords: transforming growth factor-β-stimulated clone-22,bromodomain-containing protein 7,erk pathway,ovarian cancer
                Data availability:
                Keywords: transforming growth factor-β-stimulated clone-22, bromodomain-containing protein 7, erk pathway, ovarian cancer

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