LncRNA TUSC7 Inhibits Cell Proliferation in Chronic Lymphocytic Leukemia by Modulating the miR-211-5p/SLC37A3 Axis.

Xu-Li Wang, Jia Mei
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Abstract

Chronic lymphocytic leukemia (CLL) is a malignant lymphoproliferative disorder. Long non-coding RNAs (lncRNAs) have been implicated in various regulatory processes and cancer development. Among these, lncRNA tumor suppressor candidate 7 (TUSC7) has been identified as a tumor suppressor gene. We herein measured TUSC7 expression using RT-qPCR and investigated its biological role in CLL through gain-of-function experiments. Our results revealed that TUSC7 expression was significantly lower in CLL patients compared to healthy controls, and its downregulation was associated with poor prognosis. Meanwhile, TUSC7 overexpression inhibited cell proliferation while promoting cell apoptosis. Mechanistically, TUSC7 interacted with miR-211-5p, thereby regulating the downstream target gene, solute carrier family 37 member 3 (SLC37A3). Further rescue experiments demonstrated that silencing SLC37A3 or upregulating miR-211-5p reversed the effects of TUSC7 elevation on cell proliferation and apoptosis. In conclusion, our findings suggest that TUSC7 regulates cell proliferation in CLL through the miR-211-5p/SLC37A3 axis.

LncRNA TUSC7通过调节miR-211-5p/SLC37A3轴抑制慢性淋巴细胞白血病细胞增殖。
慢性淋巴细胞白血病(CLL)是一种恶性淋巴细胞增生性疾病。长链非编码rna (lncRNAs)参与多种调控过程和癌症发展。其中,lncRNA肿瘤抑制候选基因7 (TUSC7)已被鉴定为肿瘤抑制基因。我们使用RT-qPCR检测TUSC7的表达,并通过功能获得实验研究其在CLL中的生物学作用。我们的研究结果显示,与健康对照组相比,CLL患者的TUSC7表达明显降低,其下调与预后不良有关。同时,TUSC7过表达抑制细胞增殖,促进细胞凋亡。在机制上,TUSC7与miR-211-5p相互作用,从而调节下游靶基因,溶质载体家族37成员3 (SLC37A3)。进一步的抢救实验表明,沉默SLC37A3或上调miR-211-5p可逆转TUSC7升高对细胞增殖和凋亡的影响。总之,我们的研究结果表明,TUSC7通过miR-211-5p/SLC37A3轴调节CLL细胞增殖。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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