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      The expression of heat shock protein A12B (HSPA12B) in non-Hodgkin’s lymphomas

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          Abstract

          Background

          Heat shock protein A12B (HSPA12B) plays a considerable protective role for cells, tissues, and organs against various noxious conditions. However, the expression of HSPA12B in cancer biology remains controversial. This study aimed to investigate the expression of HSPA12B and its role in cell adhesion mediated drug resistance (CAM-DR) of non-Hodgkin’s lymphoma (NHL).

          Methods

          In this study, the expression of HSPA12B in NHL was determined by immunohistochemical, and the effect of HSPA12B expression on the prognosis of NHL was analyzed by Kaplan–Meier curves. Then, the transfection technique was used to research the effect of HSPA12B in cell apoptosis. The most important was to study the expression changes of HSPA12B in the adhesion model and the effect of overexpression of HSPA12B on CAM-DR.

          Results

          We analyzed the relationship between the expression levels of HSPA12B and clinical parameters in NHL. The expression of HSPA12B was directly related to the different NHL variants. We overexpressed HSPA12B in 2 NHL cell lines and found a subsequent reduction in apoptosis. More specifically, we used an adhesion assay to demonstrate that HSPA12B expression was induced in NHL cells when they adhered to fibronectin (FN) or bone marrow stroma cells (BMSCs). Finally, it was revealed that HSPA12B overexpression enhances CAM-DR.

          Conclusions

          Our data suggest that HSPA12B may play a functional role in CAM-DR and is thus a potential novel target for NHL treatment.

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          Most cited references44

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          The microenvironment in mature B-cell malignancies: a target for new treatment strategies.

          Andreas Rosenwald, R Burger, Federico Caligaris-Cappio … (2009)
          Despite major therapeutic advances, most mature B-cell malignancies remain incurable. Compelling evidence suggests that crosstalk with accessory stromal cells in specialized tissue microenvironments, such as the bone marrow and secondary lymphoid organs, favors disease progression by promoting malignant B-cell growth and drug resistance. Therefore, disrupting the crosstalk between malignant B cells and their milieu is an attractive novel strategy for treating selected mature B-cell malignancies. Here we summarize the current knowledge about the cellular and molecular interactions between neoplastic B lymphocytes and accessory cells that shape a supportive microenvironment, and the potential therapeutic targets that are emerging, together with the new problems they raise. We discuss clinically relevant aspects and provide an outlook into future biologically oriented therapeutic strategies. We anticipate a paradigm shift in the treatment of selected B-cell malignancies, moving from targeting primarily the malignant cells toward combining cytotoxic drugs with agents that interfere with the microenvironment's proactive role. Such approaches hopefully will help eliminating residual disease, thereby improving our current therapeutic efforts.
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            Microenvironment drug resistance in multiple myeloma: emerging new players

            Lucia Di Marzo, Vanessa Desantis, Antonio Solimando … (2016)
            Multiple myeloma (MM) drug resistance (DR) is a multistep transformation process based on a powerful interplay between bone marrow stromal cells and MM cells that allows the latter to escape anti-myeloma therapies. Here we present an overview of the role of the bone marrow microenvironment in both soluble factors-mediated drug resistance (SFM-DR) and cell adhesion-mediated drug resistance (CAM-DR), focusing on the role of new players, namely miRNAs, exosomes and cancer-associated fibroblasts.
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              Extranodal dissemination of non-Hodgkin lymphoma requires CD47 and is inhibited by anti-CD47 antibody therapy.

              Mark P Chao, Chad Tang, Russell Pachynski … (2011)
              Non-Hodgkin lymphoma (NHL) presents as both localized and disseminated disease with spread to secondary sites carrying a worse prognosis. Although pathways driving NHL dissemination have been identified, there are few therapies capable of inhibiting them. Here, we report a novel role for the immunomodulatory protein CD47 in NHL dissemination, and we demonstrate that therapeutic targeting of CD47 can prevent such spread. We developed 2 in vivo lymphoma metastasis models using Raji cells, a human NHL cell line, and primary cells from a lymphoma patient. CD47 expression was required for Raji cell dissemination to the liver in mouse xenotransplants. Targeting of CD47 with a blocking antibody inhibited Raji cell dissemination to major organs, including the central nervous system, and inhibited hematogenous dissemination of primary lymphoma cells. We hypothesized that anti-CD47 antibody-mediated elimination of circulating tumor cells occurred through phagocytosis, a previously described mechanism for blocking anti-CD47 antibodies. As predicted, inhibition of dissemination by anti-CD47 antibodies was dependent on blockade of phagocyte SIRPα and required macrophage effector cells. These results demonstrate that CD47 is required for NHL dissemination, which can be therapeutically targeted with a blocking anti-CD47 antibody. Ultimately, these findings are potentially applicable to the dissemination and metastasis of other solid tumors.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Ann Transl Med
                Journal ID (iso-abbrev): Ann Transl Med
                Journal ID (publisher-id): ATM
                Title: Annals of Translational Medicine
                Publisher: AME Publishing Company
                ISSN (Print): 2305-5839
                ISSN (Electronic): 2305-5847
                Publication date (Print and electronic): September 2021
                Publication date (Print): September 2021
                Volume: 9
                Issue: 18
                Electronic Location Identifier: 1462
                Affiliations
                [1 ]Department of Medical Oncology, Affiliated Tumor Hospital of Nantong University, Nantong , China;
                [2 ]Medical School of Nantong University, Nantong , China;
                [3 ]Department of Orthopaedics, Affiliated Hospital of Nantong University, Nantong , China;
                [4 ]Department of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong , China
                Author notes

                Contributions: (I) Conception and design: S Ju; (II) Administrative support: L Yang; (III) Provision of study materials or patients: L Yang, C Peng; (IV) Collection and assembly of data: S Wang, F Yang, Q Wang; (V) Data analysis and interpretation: Y Huang, J Tang, L Zhou; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

                [#]

                These authors contributed equally to this work.

                Correspondence to: Shaoqing Ju. Department of Laboratory Medicine, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong 226001, China. Email: jsq814@ 123456hotmail.com ; Lei Yang. Department of Medical Oncology, Affiliated Tumor Hospital of Nantong University, Nantong 226361, China. Email: leiyang.53@ 123456163.com .
                Article
                Publisher ID: atm-09-18-1462
                DOI: 10.21037/atm-21-4185
                PMC ID: 8506729
                PubMed ID: 34734014
                SO-VID: 7b6d0d4d-3cfc-4269-870e-e5428fad9003
                Copyright © 2021 Annals of Translational Medicine. All rights reserved.
                License:

                Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

                History
                Date received : 30 July 2021
                Date accepted : 10 September 2021
                Categories
                Subject: Original Article

                Keywords: non-hodgkin’s lymphoma (nhl),heat shock protein a12b (hspa12b),immunohistochemistry,cell adhesion mediated drug resistance (cam-dr)
                Data availability:
                Keywords: non-hodgkin’s lymphoma (nhl), heat shock protein a12b (hspa12b), immunohistochemistry, cell adhesion mediated drug resistance (cam-dr)

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