11
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      TRIM family contribute to tumorigenesis, cancer development, and drug resistance

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The tripartite-motif (TRIM) family represents one of the largest classes of putative single protein RING-finger E3 ubiquitin ligases. TRIM family is involved in a variety of cellular signaling transductions and biological processes. TRIM family also contributes to cancer initiation, progress, and therapy resistance, exhibiting oncogenic and tumor-suppressive functions in different human cancer types. Moreover, TRIM family members have great potential to serve as biomarkers for cancer diagnosis and prognosis. In this review, we focus on the specific mechanisms of the participation of TRIM family members in tumorigenesis, and cancer development including interacting with dysregulated signaling pathways such as JAK/STAT, PI3K/AKT, TGF-β, NF-κB, Wnt/β-catenin, and p53 hub. In addition, many studies have demonstrated that the TRIM family are related to tumor resistance; modulate the epithelial–mesenchymal transition (EMT) process, and guarantee the acquisition of cancer stem cells (CSCs) phenotype. In the end, we havediscussed the potential of TRIM family members for cancer therapeutic targets.

          Related collections

          Most cited references282

          • Record: found
          • Abstract: not found
          • Article: not found

          On the Origin of Cancer Cells

          O WARBURG (1956)
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            New insights into the mechanisms of epithelial–mesenchymal transition and implications for cancer

            Epithelial-mesenchymal transition (EMT) is a cellular programme that is known to be crucial for embryogenesis, wound healing and malignant progression. During EMT, cell-cell and cell-extracellular matrix interactions are remodelled, which leads to the detachment of epithelial cells from each other and the underlying basement membrane, and a new transcriptional programme is activated to promote the mesenchymal fate. In the context of neoplasias, EMT confers on cancer cells increased tumour-initiating and metastatic potential and a greater resistance to elimination by several therapeutic regimens. In this Review, we discuss recent findings on the mechanisms and roles of EMT in normal and neoplastic tissues, and the cell-intrinsic signals that sustain expression of this programme. We also highlight how EMT gives rise to a variety of intermediate cell states between the epithelial and the mesenchymal state, which could function as cancer stem cells. In addition, we describe the contributions of the tumour microenvironment in inducing EMT and the effects of EMT on the immunobiology of carcinomas.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Wnt/β-Catenin Signaling, Disease, and Emerging Therapeutic Modalities.

              The WNT signal transduction cascade is a main regulator of development throughout the animal kingdom. Wnts are also key drivers of most types of tissue stem cells in adult mammals. Unsurprisingly, mutated Wnt pathway components are causative to multiple growth-related pathologies and to cancer. Here, we describe the core Wnt/β-catenin signaling pathway, how it controls stem cells, and contributes to disease. Finally, we discuss strategies for Wnt-based therapies.
                Bookmark

                Author and article information

                Contributors
                xuemzhang@fudan.edu.cn
                chenqian2010@sohu.com
                xinhong@fudan.edu.cn
                Journal
                Exp Hematol Oncol
                Exp Hematol Oncol
                Experimental Hematology & Oncology
                BioMed Central (London )
                2162-3619
                19 October 2022
                19 October 2022
                2022
                : 11
                : 75
                Affiliations
                [1 ]GRID grid.8547.e, ISNI 0000 0001 0125 2443, Department of Pharmacology, School of Pharmacy & General Surgery of Minhang Hospital, , Fudan University, ; Shanghai, 201203 China
                [2 ]PharmaLegacy Laboratories Co.,Ltd, Shengrong Road No.388, Zhangjiang High-tech Park, Pudong New Area, Shanghai, China
                Article
                322
                10.1186/s40164-022-00322-w
                9583506
                36261847
                f2592ba1-1bc9-4175-bbb5-c0d2ee62aeae
                © The Author(s) 2022

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 1 August 2022
                : 16 September 2022
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100007219, Natural Science Foundation of Shanghai;
                Award ID: No. 20ZR140710
                Award ID: No. 20ZR140710
                Award ID: No. 20ZR140710
                Award ID: No. 20ZR140710
                Award ID: No. 20ZR140710
                Award ID: No. 20ZR140710
                Award ID: No. 20ZR140710
                Award Recipient :
                Categories
                Review
                Custom metadata
                © The Author(s) 2022

                Oncology & Radiotherapy
                trim family,cancer,tumorigenesis,cancer resistance,signaling pathway,emt,cscs
                Oncology & Radiotherapy
                trim family, cancer, tumorigenesis, cancer resistance, signaling pathway, emt, cscs

                Comments

                Comment on this article