Wang Xu-Li, Mei Jia
Department of Hematology, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Department of Pathology, the Second Hospital of Nanjing, Affiliated to Nanjing University of Chinese Medicine, Nanjing, China.
Kaohsiung J Med Sci. 2025 May;41(5):e70003. doi: 10.1002/kjm2.70003. Epub 2025 Mar 8.
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.
慢性淋巴细胞白血病(CLL)是一种恶性淋巴细胞增殖性疾病。长链非编码RNA(lncRNAs)参与了各种调控过程和癌症发展。其中,lncRNA肿瘤抑制候选基因7(TUSC7)已被鉴定为一种肿瘤抑制基因。我们在此使用RT-qPCR检测了TUSC7的表达,并通过功能获得实验研究了其在CLL中的生物学作用。我们的结果显示,与健康对照相比,CLL患者中TUSC7的表达显著降低,其下调与预后不良相关。同时,TUSC7过表达抑制细胞增殖,同时促进细胞凋亡。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)。进一步的挽救实验表明,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中的细胞增殖。