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      Roles of N 6-methyladenosine (m 6A) modifications in gynecologic cancers: mechanisms and therapeutic targeting

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          Abstract

          Uterine and ovarian cancers are the most common gynecologic cancers. N 6−methyladenosine (m 6A), an important internal RNA modification in higher eukaryotes, has recently become a hot topic in epigenetic studies. Numerous studies have revealed that the m 6A-related regulatory factors regulate the occurrence and metastasis of tumors and drug resistance through various mechanisms. The m 6A-related regulatory factors can also be used as therapeutic targets and biomarkers for the early diagnosis of cancers, including gynecologic cancers. This review discusses the role of m 6A in gynecologic cancers and summarizes the recent advancements in m 6A modification in gynecologic cancers to improve the understanding of the occurrence, diagnosis, treatment, and prognosis of gynecologic cancers.

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          Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries

          Hyuna Sung, Jacques Ferlay, Rebecca Siegel … (2021)
          This article provides an update on the global cancer burden using the GLOBOCAN 2020 estimates of cancer incidence and mortality produced by the International Agency for Research on Cancer. Worldwide, an estimated 19.3 million new cancer cases (18.1 million excluding nonmelanoma skin cancer) and almost 10.0 million cancer deaths (9.9 million excluding nonmelanoma skin cancer) occurred in 2020. Female breast cancer has surpassed lung cancer as the most commonly diagnosed cancer, with an estimated 2.3 million new cases (11.7%), followed by lung (11.4%), colorectal (10.0 %), prostate (7.3%), and stomach (5.6%) cancers. Lung cancer remained the leading cause of cancer death, with an estimated 1.8 million deaths (18%), followed by colorectal (9.4%), liver (8.3%), stomach (7.7%), and female breast (6.9%) cancers. Overall incidence was from 2-fold to 3-fold higher in transitioned versus transitioning countries for both sexes, whereas mortality varied <2-fold for men and little for women. Death rates for female breast and cervical cancers, however, were considerably higher in transitioning versus transitioned countries (15.0 vs 12.8 per 100,000 and 12.4 vs 5.2 per 100,000, respectively). The global cancer burden is expected to be 28.4 million cases in 2040, a 47% rise from 2020, with a larger increase in transitioning (64% to 95%) versus transitioned (32% to 56%) countries due to demographic changes, although this may be further exacerbated by increasing risk factors associated with globalization and a growing economy. Efforts to build a sustainable infrastructure for the dissemination of cancer prevention measures and provision of cancer care in transitioning countries is critical for global cancer control.
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            Understanding the Warburg effect: the metabolic requirements of cell proliferation.

            Craig B Thompson, Matthew Vander Heiden, Lewis Cantley (2009)
            In contrast to normal differentiated cells, which rely primarily on mitochondrial oxidative phosphorylation to generate the energy needed for cellular processes, most cancer cells instead rely on aerobic glycolysis, a phenomenon termed "the Warburg effect." Aerobic glycolysis is an inefficient way to generate adenosine 5'-triphosphate (ATP), however, and the advantage it confers to cancer cells has been unclear. Here we propose that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass (e.g., nucleotides, amino acids, and lipids) needed to produce a new cell. Supporting this idea are recent studies showing that (i) several signaling pathways implicated in cell proliferation also regulate metabolic pathways that incorporate nutrients into biomass; and that (ii) certain cancer-associated mutations enable cancer cells to acquire and metabolize nutrients in a manner conducive to proliferation rather than efficient ATP production. A better understanding of the mechanistic links between cellular metabolism and growth control may ultimately lead to better treatments for human cancer.
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              Cancer statistics, 2016.

              Rebecca L Siegel, Kimberly D Miller, Ahmedin Jemal (2016)
              Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival. Incidence data were collected by the National Cancer Institute (Surveillance, Epidemiology, and End Results [SEER] Program), the Centers for Disease Control and Prevention (National Program of Cancer Registries), and the North American Association of Central Cancer Registries. Mortality data were collected by the National Center for Health Statistics. In 2016, 1,685,210 new cancer cases and 595,690 cancer deaths are projected to occur in the United States. Overall cancer incidence trends (13 oldest SEER registries) are stable in women, but declining by 3.1% per year in men (from 2009-2012), much of which is because of recent rapid declines in prostate cancer diagnoses. The cancer death rate has dropped by 23% since 1991, translating to more than 1.7 million deaths averted through 2012. Despite this progress, death rates are increasing for cancers of the liver, pancreas, and uterine corpus, and cancer is now the leading cause of death in 21 states, primarily due to exceptionally large reductions in death from heart disease. Among children and adolescents (aged birth-19 years), brain cancer has surpassed leukemia as the leading cause of cancer death because of the dramatic therapeutic advances against leukemia. Accelerating progress against cancer requires both increased national investment in cancer research and the application of existing cancer control knowledge across all segments of the population.
              Article 0 comments Cited 1845 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Bing Wei: m1351565@163.com
                Yunxia Cao: caoyunxia5972@ahmu.edu.cn
                Lei Zhan: 499329901@qq.com
                Journal
                Journal ID (nlm-ta): Exp Hematol Oncol
                Journal ID (iso-abbrev): Exp Hematol Oncol
                Title: Experimental Hematology & Oncology
                Publisher: BioMed Central (London )
                ISSN (Electronic): 2162-3619
                Publication date (Electronic): 12 November 2022
                Publication date PMC-release: 12 November 2022
                Publication date Collection: 2022
                Volume: 11
                Electronic Location Identifier: 98
                Affiliations
                [1 ]GRID grid.452696.a, ISNI 0000 0004 7533 3408, Obstetrics and Gynecology, , The Second Affiliated Hospital of Anhui Medical University, ; No. 678 Furong Road, Hefei, 230601 Anhui China
                [2 ]GRID grid.412679.f, ISNI 0000 0004 1771 3402, Department of Obstetrics and Gynecology, , The First Affiliated Hospital of Anhui Medical University, ; No. 218 Jixi Road, Hefei, 230022 Anhui China
                Article
                Publisher ID: 357
                DOI: 10.1186/s40164-022-00357-z
                PMC ID: 9652818
                PubMed ID: 36371254
                SO-VID: 25886558-2f32-4fc4-8256-d6a495e812d7
                Copyright © © The Author(s) 2022
                License:

                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
                Date received : 15 June 2022
                Date accepted : 1 November 2022
                Funding
                Funded by: National Nature Science Foundation of China
                Award ID: 81802586
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2022

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: n6-methyladenosine,gynecologic cancer,tumor microenvironment,prognosis,treatment
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: n6-methyladenosine, gynecologic cancer, tumor microenvironment, prognosis, treatment

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