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Long noncoding RNA small nucleolar RNA host gene 15 deteriorates liver cancer via microRNA ‐18b‐5p/ LIM‐only 4 axis
IUBMB Life ( IF 3.7 ) Pub Date : 2020-12-28 , DOI: 10.1002/iub.2431
Wei Chen 1 , Li Huang 2 , Junhua Liang 1 , Yingjian Ye 1 , Sihao Yu 1 , Yijing Zhang 1
Affiliation  

Extensive studies have explored the involvements of long noncoding RNAs (lncRNAs) in liver cancer. Limitedly, the concrete function of lncRNA small nucleolar RNA host gene 15 (SNHG15) is still elusive. Therefore, the work was initiated to unearth SNHG15-oriented mechanism in liver cancer. Liver cancer tissues were resected. The connection between SNHG15 expression with prognosis and clinicopathological traits of liver cancer patients was evaluated. Liver cancer cells SMMC-7721 were transfected with restored microRNA (miR)-18b-5p or depleted SNHG15 to discover their effects on the proliferation, migration, invasion, cycle arrest, and apoptosis of SMMC-7721 cells. The transfected SMMC-7721 cells were injected into nude mice for further investigation. SNHG15, miR-18b-5p, and LIM-only 4 (LMO4) expressions in tissues and cells were tested. The regulatory connections among SNHG15, miR-18b-5p, and LMO4 were detected. SNHG15 and LMO4 were overexpressed while miR-18b-5p was downregulated in liver cancer tissues and cells. Up-regulated SNHG15 was connected with inferior prognosis and aggressive behaviors of liver cancer patients. SNHG15 knockdown or miR-18b-5p restoration depressed SMMC-7721 cell growth in vivo and in vitro. SNHG15 bound to miR-18b-5p and miR-18b-5p targeted LMO4. The work has illuminated that silencing SNHG15 represses liver cancer progression by modulating miR-18b-5p and LMO4, indicating the therapeutic potency of SNHG15/miR-18b-5p/LMO4 axis in liver cancer.

中文翻译:

长链非编码 RNA 小核仁 RNA 宿主基因 15 通过 microRNA ‐18b-5p/ LIM-only 4 轴恶化肝癌

广泛的研究探索了长链非编码 RNA (lncRNA) 在肝癌中的作用。有限地,lncRNA小核仁RNA宿主基因15(SNHG15)的具体功能仍然难以捉摸。因此,开始了研究肝癌中 SNHG15 导向机制的工作。切除肝癌组织。评估了 SNHG15 表达与肝癌患者预后和临床病理特征之间的关系。用恢复的 microRNA (miR)-18b-5p 或耗尽的 SNHG15 转染肝癌细胞 SMMC-7721,以发现它们对 SMMC-7721 细胞增殖、迁移、侵袭、周期停滞和凋亡的影响。将转染的 SMMC-7721 细胞注射到裸鼠体内进行进一步研究。检测了组织和细胞中 SNHG15、miR-18b-5p 和仅 LIM 4 (LMO4) 的表达。检测到 SNHG15、miR-18b-5p 和 LMO4 之间的调控联系。SNHG15 和 LMO4 过表达,而 miR-18b-5p 在肝癌组织和细胞中下调。上调的 SNHG15 与肝癌患者的不良预后和攻击行为有关。SNHG15 敲低或 miR-18b-5p 恢复抑制了 SMMC-7721 细胞在体内和体外的生长。SNHG15 与 miR-18b-5p 结合,miR-18b-5p 靶向 LMO4。这项工作阐明了沉默 SNHG15 通过调节 miR-18b-5p 和 LMO4 抑制肝癌进展,表明 SNHG15/miR-18b-5p/LMO4 轴在肝癌中的治疗效力。上调的 SNHG15 与肝癌患者的不良预后和攻击行为有关。SNHG15 敲低或 miR-18b-5p 恢复抑制了 SMMC-7721 细胞在体内和体外的生长。SNHG15 与 miR-18b-5p 结合,miR-18b-5p 靶向 LMO4。这项工作阐明了沉默 SNHG15 通过调节 miR-18b-5p 和 LMO4 抑制肝癌进展,表明 SNHG15/miR-18b-5p/LMO4 轴在肝癌中的治疗效力。上调的 SNHG15 与肝癌患者的不良预后和攻击行为有关。SNHG15 敲低或 miR-18b-5p 恢复抑制了 SMMC-7721 细胞在体内和体外的生长。SNHG15 与 miR-18b-5p 结合,miR-18b-5p 靶向 LMO4。这项工作阐明了沉默 SNHG15 通过调节 miR-18b-5p 和 LMO4 抑制肝癌进展,表明 SNHG15/miR-18b-5p/LMO4 轴在肝癌中的治疗效力。
更新日期:2020-12-28
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