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FAM19A5/S1PR1 信号通路调节套细胞淋巴瘤的活力和增殖。

FAM19A5/S1PR1 signaling pathway regulates the viability and proliferation of mantle cell lymphoma.

机构信息

Department of Hematology, Lymphoma Research Center, Peking University Third Hospital, Beijing, China.

出版信息

J Recept Signal Transduct Res. 2022 Jun;42(3):225-229. doi: 10.1080/10799893.2021.1895220. Epub 2021 Mar 9.

DOI:10.1080/10799893.2021.1895220
PMID:33685344
Abstract

Several intracellular pathological processes have been reported to be regulated by the FAM19A5/S1PR1 signaling pathway. However, the role of FAM19A5/S1PR1 signaling pathway in the viability and proliferation of mantle cell lymphoma is not been completely understood. The task of this study is to explore the influence of FAM19A5/S1PR1 signaling pathway in affecting the survival and growth of mantle cell lymphoma. shRNAs against FAM19A5 or S1PR1 were transfected into mantle cell lymphom. Cell viability and proliferation were measured through MTT assay and CCK8 assay, respectively. Our results demonstrated that loss of FAM19A5 significantly reduced the viability of mantle cell lymphom, an effect that was followed by a drop in cell proliferation capacity. Besides, inhibition of S1PR1 also impairs cell survival and interrupt mantle cell lymphom proliferation . Taken together, our results illustrate that FAM19A5/S1PR1 signaling pathway is associated with the regulation of mantle cell lymphom viability and proliferation. This finding will provide a potential target for the treatment of malignant lymphoma in the clinical practice.

摘要

已有研究报道,几种细胞内病理过程受 FAM19A5/S1PR1 信号通路调控。然而,FAM19A5/S1PR1 信号通路在套细胞淋巴瘤存活和增殖中的作用尚未完全阐明。本研究旨在探讨 FAM19A5/S1PR1 信号通路对套细胞淋巴瘤存活和生长的影响。通过 shRNA 转染敲低 FAM19A5 或 S1PR1,分别采用 MTT 法和 CCK8 法检测细胞活力和增殖。结果表明,敲低 FAM19A5 可显著降低套细胞淋巴瘤的活力,进而降低细胞增殖能力。此外,抑制 S1PR1 也会损害细胞存活并阻断套细胞淋巴瘤的增殖。综上,本研究表明 FAM19A5/S1PR1 信号通路与套细胞淋巴瘤的活力和增殖调节有关。这一发现为临床恶性淋巴瘤的治疗提供了一个潜在的靶点。

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