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      TRPM2 promotes pancreatic cancer by PKC/MAPK pathway

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          Abstract

          The mechanism of pancreatic cancer (PA) is not fully understanded. In our last report, TRPM2 plays a promising role in pancreatic cancer. However, the mechanism of TRPM2 is still unknown in this dismal disease. This study was designed to investigate the role and mechanism of TRPM2 in pancreatic cancer. TRPM2 overexpressed and siRNA plasmid were created and transfected with pancreatic cancer cell line (BxPC-3) to construct the cell model. We employed CCK-8, Transwell, scratch wound, and nude mice tumor-bearing model to investigate the role of TRPM2 in pancreatic cancer. Besides, we collected the clinical data, tumor tissue sample (TT) and para-tumor sample (TP) from the pancreatic cancer patients treated in our hospital. We analyzed the mechanism of TRPM2 in pancreatic cancer by transcriptome analysis, western blot, and PCR. We blocked the downstream PKC/MEK pathway of TRPM2 to investigate the mechanism of TRPM2 in pancreatic cancer by CCK8, scratch wound healing, and transwell assays. Overexpressed TRPM2 could promote pancreatic cancer in proliferation, migration, and invasion ability in no matter the cell model or nude mice tumor-bearing model. TRPM2 level is highly negative correlated to the overall survival and progression-free survival time in PA patients, however, it is significantly increased in PA tissue as the tumor stage increases. The transcriptome analysis, GSEA analysis, western-blot, and PCR results indicate TRPM2 is highly correlated with PKC/MAPK pathways. The experiments of PKC/MEK inhibitors added to TRPM2 overexpressed BxPC-3 cell showed that significant inhibition of PA cells happened in CCK8, transwell, and wound-healing assay. TRPM2 may directly activate PKCα by calcium or indirectly activate PKCε and PKCδ by increased DAG in PA, which promote PA by downstream MAPK/MEK pathway activation.

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          Cancer statistics, 2018

          Kimberly D Miller, Rebecca Siegel, Ahmedin Jemal (2018)
          Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the United States and compiles the most recent data on cancer incidence, mortality, and survival. Incidence data, available through 2014, were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data, available through 2015, were collected by the National Center for Health Statistics. In 2018, 1,735,350 new cancer cases and 609,640 cancer deaths are projected to occur in the United States. Over the past decade of data, the cancer incidence rate (2005-2014) was stable in women and declined by approximately 2% annually in men, while the cancer death rate (2006-2015) declined by about 1.5% annually in both men and women. The combined cancer death rate dropped continuously from 1991 to 2015 by a total of 26%, translating to approximately 2,378,600 fewer cancer deaths than would have been expected if death rates had remained at their peak. Of the 10 leading causes of death, only cancer declined from 2014 to 2015. In 2015, the cancer death rate was 14% higher in non-Hispanic blacks (NHBs) than non-Hispanic whites (NHWs) overall (death rate ratio [DRR], 1.14; 95% confidence interval [95% CI], 1.13-1.15), but the racial disparity was much larger for individuals aged <65 years (DRR, 1.31; 95% CI, 1.29-1.32) compared with those aged ≥65 years (DRR, 1.07; 95% CI, 1.06-1.09) and varied substantially by state. For example, the cancer death rate was lower in NHBs than NHWs in Massachusetts for all ages and in New York for individuals aged ≥65 years, whereas for those aged <65 years, it was 3 times higher in NHBs in the District of Columbia (DRR, 2.89; 95% CI, 2.16-3.91) and about 50% higher in Wisconsin (DRR, 1.78; 95% CI, 1.56-2.02), Kansas (DRR, 1.51; 95% CI, 1.25-1.81), Louisiana (DRR, 1.49; 95% CI, 1.38-1.60), Illinois (DRR, 1.48; 95% CI, 1.39-1.57), and California (DRR, 1.45; 95% CI, 1.38-1.54). Larger racial inequalities in young and middle-aged adults probably partly reflect less access to high-quality health care. CA Cancer J Clin 2018;68:7-30. © 2018 American Cancer Society.
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            Fundamentals of cancer metabolism

            Ralph DeBerardinis, Navdeep Chandel (2016)
            Researchers provide a conceptual framework to understand current knowledge of the fundamentals of cancer metabolism.
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              Pancreatic Adenocarcinoma

              David P. Ryan, Theodore Hong, Nabeel Bardeesy (2014)
              Article 0 comments Cited 442 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Rui Lin:
                ORCID: http://orcid.org/0000-0002-3197-9798
                blackchimney@tongji.edu.cn
                Baomin Shi:
                ORCID: http://orcid.org/0000-0001-8791-569X
                baominsph@163.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): 7 June 2021
                Publication date PMC-release: 7 June 2021
                Publication date Collection: June 2021
                Volume: 12
                Issue: 6
                Electronic Location Identifier: 585
                Affiliations
                [1 ]GRID grid.24516.34, ISNI 0000000123704535, General Surgery Department, , Tongji Hospital, School of Medicine, Tongji University, ; Shanghai, 200092 China
                [2 ]GRID grid.186775.a, ISNI 0000 0000 9490 772X, School of Life Science, , Anhui Medical University, ; Hefei, 230022 China
                [3 ]GRID grid.8547.e, ISNI 0000 0001 0125 2443, School of Life Sciences, , Fudan University, ; Shanghai, 200438 China
                [4 ]GRID grid.24516.34, ISNI 0000000123704535, Shanghai Pulmonary Hospital, , School of Medicine, Tongji University, ; Shanghai, 200082 China
                Author information
                http://orcid.org/0000-0002-3197-9798
                http://orcid.org/0000-0002-6085-7319
                http://orcid.org/0000-0003-4800-8987
                http://orcid.org/0000-0001-8791-569X
                Article
                Publisher ID: 3856
                DOI: 10.1038/s41419-021-03856-9
                PMC ID: 8184946
                PubMed ID: 34099637
                SO-VID: b5e6f229-3381-4301-b0c7-f2ba945b13de
                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 : 17 November 2020
                Date revision received : 20 May 2021
                Date accepted : 20 May 2021
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2021

                ScienceOpen disciplines: Cell biology
                Keywords: cancer,molecular biology
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: cancer, molecular biology

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