For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
12
views
30
references
 Top references
cited by
13
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      198
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Estrogen receptor-α-miR-1271-SNAI2 feedback loop regulates transforming growth factor-β-induced breast cancer progression

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      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

          Background

          Breast cancer is the most common cancer among women worldwide, and approximately 70% of breast cancers are hormone receptor-positive and express estrogen receptor-α (ERα) or/and progesterone receptor. ERα has been identified to promote the growth of primary breast cancer, however, it can also antagonize signaling pathways that lead to epithelial-mesenchymal transition (EMT), including transforming growth factor-β (TGF-β) signaling. miRNA alteration or dysfunction is involved in cancer development and progression. Although miR-1271 has identified as a tumor suppressor in various cancers, the role of miR-1271 in breast cancer is still limited.

          Methods

          The effect of miR-1271 on breast cancer progression was investigated both in vitro and in vivo. The EMT-related protein expression levels and localization were analyzed by western blotting and immunofluorescence, respectively. Chromatin immunoprecipitation and dual-luciferase reporter assays were used to validate the regulation of ERα-miR-1271-SNAI2 feedback loop.

          Results

          miR-1271 suppresses breast cancer progression and EMT phenotype both in vitro and in vivo by targeting SNAI2. Estrogen reverses TGF-β-induced EMT in a miR-1271 dependent manner. Furthermore, ERα transactivates the miR-1271 expression and is also transcriptionally repressed by SNAI2.

          Conclusions

          Our data uncover the ERα-miR-1271-SNAI2 feedback loop and provide a mechanism to explain the TGF-β network in breast cancer progression.

          Electronic supplementary material

          The online version of this article (10.1186/s13046-019-1112-4) contains supplementary material, which is available to authorized users.

          Related collections

          Most cited references30

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Induction of metastasis, cancer stem cell phenotype, and oncogenic metabolism in cancer cells by ionizing radiation

          Su-Yeon Lee, Eui-Kyong Jeong, Min Kyung Ju … (2017)
          Radiation therapy is one of the major tools of cancer treatment, and is widely used for a variety of malignant tumours. Radiotherapy causes DNA damage directly by ionization or indirectly via the generation of reactive oxygen species (ROS), thereby destroying cancer cells. However, ionizing radiation (IR) paradoxically promotes metastasis and invasion of cancer cells by inducing the epithelial-mesenchymal transition (EMT). Metastasis is a major obstacle to successful cancer therapy, and is closely linked to the rates of morbidity and mortality of many cancers. ROS have been shown to play important roles in mediating the biological effects of IR. ROS have been implicated in IR-induced EMT, via activation of several EMT transcription factors—including Snail, HIF-1, ZEB1, and STAT3—that are activated by signalling pathways, including those of TGF-β, Wnt, Hedgehog, Notch, G-CSF, EGFR/PI3K/Akt, and MAPK. Cancer cells that undergo EMT have been shown to acquire stemness and undergo metabolic changes, although these points are debated. IR is known to induce cancer stem cell (CSC) properties, including dedifferentiation and self-renewal, and to promote oncogenic metabolism by activating these EMT-inducing pathways. Much accumulated evidence has shown that metabolic alterations in cancer cells are closely associated with the EMT and CSC phenotypes; specifically, the IR-induced oncogenic metabolism seems to be required for acquisition of the EMT and CSC phenotypes. IR can also elicit various changes in the tumour microenvironment (TME) that may affect invasion and metastasis. EMT, CSC, and oncogenic metabolism are involved in radioresistance; targeting them may improve the efficacy of radiotherapy, preventing tumour recurrence and metastasis. This study focuses on the molecular mechanisms of IR-induced EMT, CSCs, oncogenic metabolism, and alterations in the TME. We discuss how IR-induced EMT/CSC/oncogenic metabolism may promote resistance to radiotherapy; we also review efforts to develop therapeutic approaches to eliminate these IR-induced adverse effects.
          Article 0 comments Cited 222 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Cancer screening in the United States, 2015: a review of current American cancer society guidelines and current issues in cancer screening.

            Robert A Smith, Deana Manassaram-Baptiste, Durado Brooks … (2024)
            Each year, the American Cancer Society (ACS) publishes a summary of its guidelines for early cancer detection along with a report on data and trends in cancer screening rates and select issues related to cancer screening. In this issue of the journal, we summarize current ACS cancer screening guidelines. The latest data on utilization of cancer screening from the National Health Interview Survey (NHIS) also is described, as are several issues related to screening coverage under the Affordable Care Act, including the expansion of the Medicaid program.
            Article 0 comments Cited 106 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              MicroRNAs as biomarkers for early breast cancer diagnosis, prognosis and therapy prediction.

              Rihab Nasr, Farah Nassar, Rabih Talhouk (2017)
              Breast cancer is a major health problem that affects one in eight women worldwide. As such, detecting breast cancer at an early stage anticipates better disease outcome and prolonged patient survival. Extensive research has shown that microRNA (miRNA) are dysregulated at all stages of breast cancer. miRNA are a class of small noncoding RNA molecules that can modulate gene expression and are easily accessible and quantifiable. This review highlights miRNA as diagnostic, prognostic and therapy predictive biomarkers for early breast cancer with an emphasis on the latter. It also examines the challenges that lie ahead in their use as biomarkers. Noteworthy, this review addresses miRNAs reported in patients with early breast cancer prior to chemotherapy, radiotherapy, surgical procedures or distant metastasis (unless indicated otherwise). In this context, miRNA that are mentioned in this review were significantly modulated using more than one statistical test and/or validated by at least two studies. A standardized protocol for miRNA assessment is proposed starting from sample collection to data analysis that ensures comparative analysis of data and reproducibility of results.
              Article 0 comments Cited 104 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Bo-Wen Liu: lbw5324883@126.com
                Zhi-Hao Yu: niki_y@163.com
                Ao-Xiang Chen: chen_aoxiang@126.com
                Jiang-Rui Chi: rebecca20110311@163.com
                Jie Ge: 13920339114@163.com
                Yue Yu: 86-022-23 340 123 , yuyue@tmu.edu.cn
                Xu-Chen Cao:
                ORCID: http://orcid.org/0000-0003-3216-6673
                86-022-23 340 123 , caoxuchen@tmu.edu.cn
                Journal
                Journal ID (nlm-ta): J Exp Clin Cancer Res
                Journal ID (iso-abbrev): J. Exp. Clin. Cancer Res
                Title: Journal of Experimental & Clinical Cancer Research : CR
                Publisher: BioMed Central (London )
                ISSN (Print): 0392-9078
                ISSN (Electronic): 1756-9966
                Publication date (Electronic): 1 March 2019
                Publication date PMC-release: 1 March 2019
                Publication date Collection: 2019
                Volume: 38
                Electronic Location Identifier: 109
                Affiliations
                [1 ]ISNI 0000 0004 1798 6427, GRID grid.411918.4, The First Department of Breast Cancer, , National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, ; Huan-Hu-Xi Road, Hexi District, Tianjin, 300060 China
                [2 ]ISNI 0000 0004 1798 6427, GRID grid.411918.4, Key Laboratory of Cancer Prevention and Therapy, ; Tianjin, 300060 China
                [3 ]Tianjin’s Clinical Research Center for Cancer, Tianjin, 300060 China
                [4 ]ISNI 0000 0004 0369 313X, GRID grid.419897.a, Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, , Ministry of Education, ; Tianjin, 300060 China
                Author information
                http://orcid.org/0000-0003-3216-6673
                Article
                Publisher ID: 1112
                DOI: 10.1186/s13046-019-1112-4
                PMC ID: 6397493
                PubMed ID: 30823890
                SO-VID: 530871b0-3b2a-44ff-86fc-053a20d922f7
                Copyright © © The Author(s). 2019
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

                History
                Date received : 2 January 2019
                Date accepted : 18 February 2019
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81502518
                Award ID: 81702624
                Award ID: 81502300
                Award Recipient :
                Funded by: Natural Science Foundation of Tianjin City (CN)
                Award ID: 17JCQNJC10400
                Award Recipient :
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: breast cancer,transforming growth factor-β,epithelial to mesenchymal transition,mir-1271,snai2,erα
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: breast cancer, transforming growth factor-β, epithelial to mesenchymal transition, mir-1271, snai2, erα

                Comments

                Comment on this article

                scite_

                Similar content198

                See all similar

                Cited by13

                See all cited by

                Most referenced authors408

                See all reference authors