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      Carnosic Acid Induces Antiproliferation and Anti-Metastatic Property of Esophageal Cancer Cells via MAPK Signaling Pathways

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          Abstract

          Background

          Carnosic acid (CA) is a polyphenolic diterpene extracted from rosemary. Reports have shown that CA possesses anticancer activity. However, whether CA inhibits esophageal squamous cell carcinoma, an aggressive type of esophageal cancer, remains untested.

          Methods

          The effects of CA on cell survival, migration, and apoptosis were evaluated by a combination of MTT, colony formation assay, flow cytometry, and Transwell assay. The potential signaling pathways involved were investigated via Western blot assay.

          Results

          CA dose-dependently inhibited cell proliferation, apoptosis, migration, and colony formation. Mechanistically, CA arrested the cell cycle at G2/M phase, promoted cell apoptosis, induced DNA damage, and inhibited the MAPK signaling pathways.

          Conclusion

          Our results suggest that CA is a potential anticancer drug for esophageal squamous cell carcinoma.

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          Most cited references36

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          Epithelial–mesenchymal plasticity in carcinoma metastasis

          Jeff H. Tsai, Jing Yang (2013)
          A developmental program termed epithelial–mesenchymal transition (EMT) plays a critical role in promoting metastasis in epithelial-derived carcinomas. Recent studies also implicate its reverse program, mesenchymal–epithelial transition (MET), in this metastatic process. In this review, Tsai and Yang discuss the functional requirement of EMT and/or MET during the individual steps of tumor metastasis and the potential for targeting these programs when treating metastatic diseases.
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            Immune suppressive landscape in the human esophageal squamous cell carcinoma microenvironment

            Yingxia Zheng, Zheyi Chen, Yichao Han … (2020)
            Cancer immunotherapy has revolutionized cancer treatment, and it relies heavily on the comprehensive understanding of the immune landscape of the tumor microenvironment (TME). Here, we obtain a detailed immune cell atlas of esophageal squamous cell carcinoma (ESCC) at single-cell resolution. Exhausted T and NK cells, regulatory T cells (Tregs), alternatively activated macrophages and tolerogenic dendritic cells are dominant in the TME. Transcriptional profiling coupled with T cell receptor (TCR) sequencing reveal lineage connections in T cell populations. CD8 T cells show continuous progression from pre-exhausted to exhausted T cells. While exhausted CD4, CD8 T and NK cells are major proliferative cell components in the TME, the crosstalk between macrophages and Tregs contributes to potential immunosuppression in the TME. Our results indicate several immunosuppressive mechanisms that may be simultaneously responsible for the failure of immuno-surveillance. Specific targeting of these immunosuppressive pathways may reactivate anti-tumor immune responses in ESCC.
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              Metformin induces autophagy and G0/G1 phase cell cycle arrest in myeloma by targeting the AMPK/mTORC1 and mTORC2 pathways

              Yan Wang, Wenbin Xu, Zixun Yan … (2018)
              Background Metformin is a commonly used drug for the treatment of diabetes. Accumulating evidence suggests that it exerts anti-tumor effects in many cancers, including multiple myeloma (MM); however, the underlying molecular mechanisms have not been clearly elucidated. Methods The anti-myeloma effects of metformin were evaluated using human MM cell lines (RPMI8226 and U266) in vitro and in vivo NOD-SCID murine xenograft MM model. Cell viability was assessed with CCK8 and cell proliferation was measured by EdU incorporation assay. Cell cycle distribution and apoptosis were examined by flow cytometry. Transmission electron microscopy was used to visualized autophagosomes. Activation of AMPK and inhibition of mTORC1/C2 pathways was assessed by Western blot analysis. RPMI8226 cells and U266 cell lines with AMPK knockdown were generated by transfection with small interfering RNA targeting the AMPK-α1 and α2 subunits using Lipofectamine 2000 reagent. Results Metformin effectively inhibited the proliferation of MM cell lines, an effect that was associated with the induction of autophagy and G0/G1 cell cycle arrest, but not apoptosis. Metformin activated AMPK and repressed both mTORC1 and mTORC2 signaling pathways in myeloma cells as well as downstream molecular signaling pathways, such as p-4EBP1 and p-AKT. AMPK activation resulted in direct phosphorylation and activation of tuberous sclerosis complex 2 (TSC2), leading to inhibition of the mammalian target of rapamycin (mTOR). In addition, metformin inhibited myeloma cell growth in an AMPK-dependent manner. The xenograft mouse model further confirmed that metformin inhibited tumor growth by upregulation of AMPK and downregulation of mTOR. Conclusions Metformin inhibits the proliferation of myeloma cells by inducing autophagy and cell-cycle arrest. Our results suggest that the molecular mechanism involves dual repression of mTORC1 and mTORC2 pathways via AMPK activation. Our study provides a theoretical basis for the development of novel strategies for the treatment of MM using metformin as an already approved and safe drug.
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                Author and article information

                Contributors
                Zhiqiang Zhan:
                ORCID: https://orcid.org/0000-0003-0232-8328
                Journal
                Journal ID (nlm-ta): J Oncol
                Journal ID (iso-abbrev): J Oncol
                Journal ID (publisher-id): jo
                Title: Journal of Oncology
                Publisher: Hindawi
                ISSN (Print): 1687-8450
                ISSN (Electronic): 1687-8469
                Publication date Collection: 2021
                Publication date (Electronic): 16 November 2021
                Volume: 2021
                Electronic Location Identifier: 4451533
                Affiliations
                1Division of Thoracic and Endocrine Surgery, University Hospitals and University of Geneva, Geneva 41211, Switzerland
                2School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, China
                3Department of Clinical Medicine, Jiangxi Health Vocational College of China, Nanchang, Jiangxi, China
                4Jiangxi Key Laboratory of Translational Cancer Research, Jiangxi Cancer Hospital of Nanchang University, Nanchang, Jiangxi, China
                5Department of Pathology, Jiangxi Cancer Hospital of Nanchang University, Nanchang, Jiangxi, China
                6Department of Thoracic Surgery, Jiangxi Cancer Hospital of Nanchang University, Nanchang, Jiangxi, China
                7Department of Oncology, Jiangxi Pingxiang People's Hospital, Pingxiang, Jiangxi, China
                Author notes

                Academic Editor: Yuan Seng Wu

                Author information
                https://orcid.org/0000-0003-0232-8328
                Article
                DOI: 10.1155/2021/4451533
                PMC ID: 8610725
                PubMed ID: 34824582
                SO-VID: 582ab8d5-aa3f-4237-aead-2518d8dfe42d
                Copyright © Copyright © 2021 Sicong Jiang et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 2 July 2021
                Date accepted : 2 November 2021
                Funding
                Funded by: Jiangxi Key Technology R&D Program Foundation
                Award ID: 2009BSB11003
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Oncology & Radiotherapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy

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