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Modulation of lymphoma growth by a selective serotonin receptor antagonist
Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Immunology/Immunchemistry.
Umeå University, Faculty of Medicine, Department of Medical Biosciences.
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2017 (English)In: Scandinavian Journal of Immunology, ISSN 0300-9475, E-ISSN 1365-3083, Vol. 86, no 4, p. 343-343Article in journal, Meeting abstract (Other academic) Published
Abstract [en]

The mitogenic neurotransmitter, serotonin (5‐HT) acts as a growth factor for different types of non‐tumoral cells (e.g. vascular smooth muscle cells) and tumor cells (e.g. pancreatic carcinoid cells). The 5‐HT1A is a prototype receptor of 5‐HT1 family and as a G‐protein coupled receptor (GPCR), it exerts inhibitory action through Gi/o subunits and activating response via βγ subunits. 5‐HT1A receptors have long been implicated in the treatment of anxiety and depressive disorders. Apart from its role in neuropsychiatric diseases, 5‐HT1A receptor mediated signaling is important for T and B cell proliferation since blocking of the receptor has been linked to a reduced in vitro proliferative response after mitogenic stimulation. Here, we investigated the phenotypical and molecular effects of serotonin signaling by treating human B cell‐derived lymphoma cell lines with a selective 5‐HT1A antagonist. Our data show that repeated treatments with the 5‐HT1A antagonist resulted in significantly reduced proliferation in human B‐derived lymphoma cell lines. We demonstrate that the block in proliferation was associated with induction of apoptosis, DNA damage and morphological alterations of surviving cells. We also provide evidence that treatment of lymphoma B cells with the 5HT1A antagonist leads to activation of GSK3‐beta and a downregulation of c‐MYC and cyclin D1 mRNA transcripts. Collectively, our data indicate that modulation of serotonin signaling may have potential for treatment of B cell‐derived lymphomas.

Place, publisher, year, edition, pages
John Wiley & Sons, 2017. Vol. 86, no 4, p. 343-343
National Category
Immunology
Identifiers
URN: urn:nbn:se:umu:diva-140898DOI: 10.1111/sji.12587ISI: 000411865200222OAI: oai:DiVA.org:umu-140898DiVA, id: diva2:1158512
Conference
44th Annual Meeting of the Scandinavian-Society-for-Immunology (SSI), Stockholm, Sweden, October 17-20, 2017
Note

Meeting Abstract: D-31412

Available from: 2017-11-20 Created: 2017-11-20 Last updated: 2020-08-03Bibliographically approved

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Kolan, Shrikant S.Lidström, TommyHultdin, MagnusForsell, Mattias

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Kolan, Shrikant S.Lidström, TommyHultdin, MagnusForsell, Mattias
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Immunology/ImmunchemistryDepartment of Medical Biosciences
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Scandinavian Journal of Immunology
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