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长非编码RNALGALS8-AS1促进血管生成和大脑转移在非小细胞肺癌

Jian Zhong¹, Bo Wang¹

¹1Department of Thoracic Surgery, Affiliated Brain Hospital of Nanjing Medical University, Nanjing City, Jiangsu Province, 210000, China; 2Department of Thoracic surgery, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing 210029, China.

Acta biochimica Polonica

|September 16, 2023

概括

长非编码RNALGAS8-AS1促进非小细胞肺癌 (NSCLC) 中的大脑转移. 抑制LGAS8-AS1可能为具有转移潜力的NSCLC患者提供新的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
癌症研究癌症研究

背景情况:

大脑转移 (BM) 显著恶化非小细胞肺癌 (NSCLC) 患者的预后.
了解驱动NSCLC中BM的分子机制对于开发有效的治疗方法至关重要.

研究的目的:

研究LGAS8-AS1在非小细胞肺癌中大脑转移的进展中的作用.
阐明通过LGAS8-AS1影响NSCLC转移的分子途径.

主要方法:

分析了60名NSCLC患者 (30名有BM,30名没有BM) 的临床数据.
在体外实验中评估了LGAS8-AS1耗尽对NSCLC细胞行为 (增殖,迁移,入侵,血管生成) 的影响.
在体内研究评估了LGAS8-AS1对NSCLC瘤发生和BM的影响.

主要成果:

与那些没有BM的患者相比,患有BM的NSCLC患者表现出明显更高的LGAS8-AS1水平.
消耗LGAS8-AS1抑制NSCLC细胞的增殖,迁移,入侵和血管生成在体外,并减少瘤生长和体内BM.
发现LGAS8-AS1针对miR-885-3p,从而调节了Fascin-actin-bundling protein 1 (FSCN1) 的表达.

结论:

通过miR-885-3p/FSCN1轴,LGAS8-AS1在促进NSCLC脑转移方面发挥着至关重要的作用.
抑制LGAS8-AS1证明了控制NSCLC转移的治疗潜力.
LGAS8-AS1可以作为一种有价值的生物标志物,用于识别患有大脑转移风险的NSCLC患者.

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