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      STAT3/LINC00671 axis regulates papillary thyroid tumor growth and metastasis via LDHA-mediated glycolysis

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          Abstract

          Lactate dehydrogenase A (LDHA), a critical component of the glycolytic pathway, relates to the development of various cancers, including thyroid cancer. However, the regulatory mechanism of LDHA inhibition and the physiological significance of the LDHA inhibitors in papillary thyroid cancer (PTC) are unknown. Long non-coding RNA (lncRNA) plays a vital role in tumor growth and progression. Here, we identified a novel lncRNA LINC00671 negatively correlated with LDHA, downregulating LDHA expression and predicting good clinical outcome in thyroid cancer. Moreover, hypoxia inhibits LINC00671 expression and activates LDHA expression largely through transcriptional factor STAT3. STAT3/LINC00671/LDHA axis regulates thyroid cancer glycolysis, growth, and lung metastasis both in vitro and in vivo. In thyroid cancer patients, LINC00671 expression is negatively correlated with LDHA and STAT3 expression. Our work established STAT3/LINC00671/LDHA as a critical axis to regulate PTC growth and progression. Inhibition of LDHA or STAT3 or supplement of LINC00671 could be potential therapeutic strategies in thyroid cancer.

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          Global Cancer Statistics 2018: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries

          Ahmedin Jemal, Lindsey A Torre, Rebecca Siegel … (2018)
          This article provides a status report on the global burden of cancer worldwide using the GLOBOCAN 2018 estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer, with a focus on geographic variability across 20 world regions. There will be an estimated 18.1 million new cancer cases (17.0 million excluding nonmelanoma skin cancer) and 9.6 million cancer deaths (9.5 million excluding nonmelanoma skin cancer) in 2018. In both sexes combined, lung cancer is the most commonly diagnosed cancer (11.6% of the total cases) and the leading cause of cancer death (18.4% of the total cancer deaths), closely followed by female breast cancer (11.6%), prostate cancer (7.1%), and colorectal cancer (6.1%) for incidence and colorectal cancer (9.2%), stomach cancer (8.2%), and liver cancer (8.2%) for mortality. Lung cancer is the most frequent cancer and the leading cause of cancer death among males, followed by prostate and colorectal cancer (for incidence) and liver and stomach cancer (for mortality). Among females, breast cancer is the most commonly diagnosed cancer and the leading cause of cancer death, followed by colorectal and lung cancer (for incidence), and vice versa (for mortality); cervical cancer ranks fourth for both incidence and mortality. The most frequently diagnosed cancer and the leading cause of cancer death, however, substantially vary across countries and within each country depending on the degree of economic development and associated social and life style factors. It is noteworthy that high-quality cancer registry data, the basis for planning and implementing evidence-based cancer control programs, are not available in most low- and middle-income countries. The Global Initiative for Cancer Registry Development is an international partnership that supports better estimation, as well as the collection and use of local data, to prioritize and evaluate national cancer control efforts. CA: A Cancer Journal for Clinicians 2018;0:1-31. © 2018 American Cancer Society.
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            Hallmarks of Cancer: The Next Generation

            Douglas Hanahan, Robert A. Weinberg (2011)
            The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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              Gene regulation by long non-coding RNAs and its biological functions

              Luisa Statello, Chun-Jie Guo, Ling-Ling Chen … (2020)
              Evidence accumulated over the past decade shows that long non-coding RNAs (lncRNAs) are widely expressed and have key roles in gene regulation. Recent studies have begun to unravel how the biogenesis of lncRNAs is distinct from that of mRNAs and is linked with their specific subcellular localizations and functions. Depending on their localization and their specific interactions with DNA, RNA and proteins, lncRNAs can modulate chromatin function, regulate the assembly and function of membraneless nuclear bodies, alter the stability and translation of cytoplasmic mRNAs and interfere with signalling pathways. Many of these functions ultimately affect gene expression in diverse biological and physiopathological contexts, such as in neuronal disorders, immune responses and cancer. Tissue-specific and condition-specific expression patterns suggest that lncRNAs are potential biomarkers and provide a rationale to target them clinically. In this Review, we discuss the mechanisms of lncRNA biogenesis, localization and functions in transcriptional, post-transcriptional and other modes of gene regulation, and their potential therapeutic applications.
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                Author and article information

                Contributors
                Nan Du:
                ORCID: http://orcid.org/0000-0001-8608-1021
                Dunan05@aliyun.com
                Lei Kang:
                ORCID: http://orcid.org/0000-0001-8729-4547
                kanglei@bjmu.edu.cn
                Xiao-jie Xu:
                ORCID: http://orcid.org/0000-0002-7337-4308
                miraclexxj@126.com
                Journal
                Journal ID (nlm-ta): Cell Death Dis
                Journal ID (iso-abbrev): Cell Death Dis
                Title: Cell Death & Disease
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2041-4889
                Publication date (Electronic): 17 August 2021
                Publication date PMC-release: 17 August 2021
                Publication date Collection: September 2021
                Volume: 12
                Issue: 9
                Electronic Location Identifier: 799
                Affiliations
                [1 ]GRID grid.43555.32, ISNI 0000 0000 8841 6246, Department of Genetic Engineering, , Beijing Institute of Biotechnology, ; Beijing, China
                [2 ]GRID grid.414252.4, ISNI 0000 0004 1761 8894, Department of Oncology, , Fourth Medical Center of PLA General Hospital, ; Beijing, China
                [3 ]GRID grid.414252.4, ISNI 0000 0004 1761 8894, Department of Paediatric Orthopaedic Surgery, , Seventh Medical Center of PLA General Hospital, ; Beijing, China
                [4 ]GRID grid.411472.5, ISNI 0000 0004 1764 1621, Department of Nuclear Medicine, , Peking University First Hospital, ; Beijing, China
                Author information
                http://orcid.org/0000-0001-9969-306X
                http://orcid.org/0000-0001-5377-4892
                http://orcid.org/0000-0001-8608-1021
                http://orcid.org/0000-0001-8729-4547
                http://orcid.org/0000-0002-7337-4308
                Article
                Publisher ID: 4081
                DOI: 10.1038/s41419-021-04081-0
                PMC ID: 8371129
                PubMed ID: 34404767
                SO-VID: e98e56ab-dbd0-41fa-ae02-b4fd2edccf66
                Copyright © © The Author(s) 2021
                License:

                Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 14 May 2021
                Date revision received : 25 July 2021
                Date accepted : 29 July 2021
                Funding
                Funded by: Beijing Science Foundation (7192196)
                Funded by: PKU Medicine-X Youth Program (No. PKU2021LCXQ023),Open Funding Project of the State Key Laboratory of Biochemical Engineering (No. 2020KF-01).
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2021

                ScienceOpen disciplines: Cell biology
                Keywords: oncogenes,cancer metabolism
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: oncogenes, cancer metabolism

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