For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
3
views
35
references
 Top references
cited by
4
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      80
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      HMGB3 promotes the malignant phenotypes and stemness of epithelial ovarian cancer through the MAPK/ERK signaling pathway

      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

          Ovarian cancer, particularly epithelial ovarian cancer (EOC), is the leading cause of cancer-related mortality among women. Our previous study revealed that high HMGB3 levels are associated with poor prognosis and lymph node metastasis in patients with high-grade serous ovarian carcinoma; however, the role of HMGB3 in EOC proliferation and metastasis remains unknown.

          Methods

          MTT, clonogenic, and EdU assays were used to assess cell proliferation. Transwell assays were performed to detect cell migration and invasion. Signaling pathways involved in HMGB3 function were identified by RNA sequencing (RNA-seq). MAPK/ERK signaling pathway protein levels were evaluated by western blot.

          Results

          HMGB3 knockdown inhibited ovarian cancer cell proliferation and metastasis, whereas HMGB3 overexpression facilitated these processes. RNA-seq showed that HMGB3 participates in regulating stem cell pluripotency and the MAPK signaling pathway. We further proved that HMGB3 promotes ovarian cancer stemness, proliferation, and metastasis through activating the MAPK/ERK signaling pathway. In addition, we demonstrated that HMGB3 promotes tumor growth in a xenograft model via MAPK/ERK signaling.

          Conclusions

          HMGB3 promotes ovarian cancer malignant phenotypes and stemness through the MAPK/ERK signaling pathway. Targeting HMGB3 is a promising strategy for ovarian cancer treatment that may improve the prognosis of women with this disease.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s12964-023-01172-7.

          Related collections

          Most cited references35

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

          Cancer statistics in China and United States, 2022: profiles, trends, and determinants

          Changfa Xia, Xuesi Dong, He. Li … (2022)
          Background: The cancer burden in the United States of America (USA) has decreased gradually. However, China is experiencing a transition in its cancer profiles, with greater incidence of cancers that were previously more common in the USA. This study compared the latest cancer profiles, trends, and determinants between China and USA. Methods: This was a comparative study using open-source data. Cancer cases and deaths in 2022 were calculated using cancer estimates from GLOBOCAN 2020 and population estimates from the United Nations. Trends in cancer incidence and mortality rates in the USA used data from the Surveillance, Epidemiology, and End Results program and National Center for Health Statistics. Chinese data were obtained from cancer registry reports. Data from the Global Burden of Disease 2019 and a decomposition method were used to express cancer deaths as the product of four determinant factors. Results: In 2022, there will be approximately 4,820,000 and 2,370,000 new cancer cases, and 3,210,000 and 640,000 cancer deaths in China and the USA, respectively. The most common cancers are lung cancer in China and breast cancer in the USA, and lung cancer is the leading cause of cancer death in both. Age-standardized incidence and mortality rates for lung cancer and colorectal cancer in the USA have decreased significantly recently, but rates of liver cancer have increased slightly. Rates of stomach, liver, and esophageal cancer decreased gradually in China, but rates have increased for colorectal cancer in the whole population, prostate cancer in men, and other seven cancer types in women. Increases in adult population size and population aging were major determinants for incremental cancer deaths, and case-fatality rates contributed to reduced cancer deaths in both countries. Conclusions: The decreasing cancer burden in liver, stomach, and esophagus, and increasing burden in lung, colorectum, breast, and prostate, mean that cancer profiles in China and the USA are converging. Population aging is a growing determinant of incremental cancer burden. Progress in cancer prevention and care in the USA, and measures to actively respond to population aging, may help China to reduce the cancer burden.
          Article 0 comments Cited 975 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            A Comprehensive Review on MAPK: A Promising Therapeutic Target in Cancer

            Cornelia Braicu, Mihail Buse, Constantin Busuioc … (2019)
            The mitogen-activated protein kinase (MAPK) pathway is an important bridge in the switch from extracellular signals to intracellular responses. Alterations of signaling cascades are found in various diseases, including cancer, as a result of genetic and epigenetic changes. Numerous studies focused on both the homeostatic and the pathologic conduct of MAPK signaling; however, there is still much to be deciphered in terms of regulation and action models in both preclinical and clinical research. MAPK has implications in the response to cancer therapy, particularly the activation of the compensatory pathways in response to experimental MAPK inhibition. The present paper discusses new insights into MAPK as a complex cell signaling pathway with roles in the sustenance of cellular normal conduit, response to cancer therapy, and activation of compensatory pathways. Unfortunately, most MAPK inhibitors trigger resistance due to the activation of compensatory feed-back loops in tumor cells and tumor microenvironment components. Therefore, novel combinatorial therapies have to be implemented for cancer management in order to restrict the possibility of alternative pathway activation, as a perspective for developing novel therapies based on integration in translational studies.
            Article 0 comments Cited 258 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              Targeting MAPK Signaling in Cancer: Mechanisms of Drug Resistance and Sensitivity

              Shannon M. Lee, Jens Rauch, Walter Kolch (2020)
              Mitogen-activated protein kinase (MAPK) pathways represent ubiquitous signal transduction pathways that regulate all aspects of life and are frequently altered in disease. Here, we focus on the role of MAPK pathways in modulating drug sensitivity and resistance in cancer. We briefly discuss new findings in the extracellular signaling-regulated kinase (ERK) pathway, but mainly focus on the mechanisms how stress activated MAPK pathways, such as p38 MAPK and the Jun N-terminal kinases (JNK), impact the response of cancer cells to chemotherapies and targeted therapies. In this context, we also discuss the role of metabolic and epigenetic aberrations and new therapeutic opportunities arising from these changes.
              Article 0 comments Cited 253 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Beihua Kong: kongbeihua@sdu.edu.cn
                Journal
                Journal ID (nlm-ta): Cell Commun Signal
                Journal ID (iso-abbrev): Cell Commun Signal
                Title: Cell Communication and Signaling : CCS
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1478-811X
                Publication date (Electronic): 16 June 2023
                Publication date PMC-release: 16 June 2023
                Publication date Collection: 2023
                Volume: 21
                Electronic Location Identifier: 144
                Affiliations
                [1 ]GRID grid.452402.5, ISNI 0000 0004 1808 3430, Department of Obstetrics and Gynecology, , Qilu Hospital of Shandong University, ; 107 Wenhua Xi Road, Jinan, 250012 China
                [2 ]GRID grid.452402.5, ISNI 0000 0004 1808 3430, Gynecologic Oncology Key Laboratory of Shandong Province, , Qilu Hospital of Shandong University, ; Jinan, 250012 China
                [3 ]GRID grid.27255.37, ISNI 0000 0004 1761 1174, School of Medicine, Cheeloo College of Medicine, , Shandong University, ; Jinan, 250012 China
                [4 ]GRID grid.452402.5, ISNI 0000 0004 1808 3430, Department of Ophthalmology, , Qilu Hospital of Shandong University, ; Jinan, 250012 China
                [5 ]71217 of the Chinese People’s Liberation Army, Laiyang, 265200 China
                Article
                Publisher ID: 1172
                DOI: 10.1186/s12964-023-01172-7
                PMC ID: 10273509
                PubMed ID: 37328851
                SO-VID: 1eb967c5-10b0-4ba4-beb7-acbfee517417
                Copyright © © The Author(s) 2023
                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 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 : 27 February 2023
                Date accepted : 21 May 2023
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100010031, Postdoctoral Research Foundation of China;
                Award ID: 2020M672070
                Funded by: Tai-Shan Scholar Program from Shandong Province
                Award ID: Nos. ts20070743
                Funded by: National Natural Science Foundation of China
                Award ID: 82072871
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © BioMed Central Ltd., part of Springer Nature 2023

                ScienceOpen disciplines: Cell biology
                Keywords: hmgb3,ovarian cancer,proliferation,stemness,mapk
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: hmgb3, ovarian cancer, proliferation, stemness, mapk

                Comments

                Comment on this article

                scite_

                Similar content80

                See all similar

                Cited by4

                See all cited by

                Most referenced authors425

                See all reference authors