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lncRNA-WAL通过诱导β-氨酸核转位促进三阴性乳腺癌的攻击性
Hongyan Huang1,2,3, Haiyun Jin4, Rong Lei2
1Department of Breast Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Molecular cancer research : MCR
|July 1, 2024
概括
三重阴性乳腺癌 (TNBC) 由于治疗耐药性而具有挑战性. 一种新的长非编码RNA,lnc-WAL,通过稳定Wnt/β-catenin通路,促进TNBC进展,提供潜在的治疗标.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 三重阴性乳腺癌 (TNBC) 对传统疗法表现出耐药性.
- 异常的Wnt/β-catenin通路激活与TNBC进展有关.
- 长非编码RNAs (lncRNAs) 越来越多地被认为是它们在癌症中的作用.
研究的目的:
- 识别和描述参与TNBC中Wnt/β-catenin通路激活的新型lncRNAs.
- 为了阐明Inc-WAL影响TNBC恶性瘤的机制.
- 评估lnc-WAL作为TNBC的潜在治疗标和预后生物标志物.
主要方法:
- lncRNA微阵列分析,以比较具有激活与非激活Wnt/β-catenin通路的TNBC组织.
- RNA免疫沉降测序 (RIP-seq) 确认了lnc-WAL和β-catenin之间的相互作用.
- 在体外测试以评估Inc-WAL对细胞增殖,迁移,入侵和上皮-介质细胞过渡 (EMT) 的影响.
主要成果:
- lnc-WAL被确定为TNBC中最高调节的lncRNA,具有激活的Wnt/β-catenin信号传递.
- lnc-WAL直接与β-catenin相互作用,并通过AXIN介导的酸化抑制其降解.
- 在瘤中增加lnc-WAL表达与患者存活时间缩短相关,并促进了TNBC细胞的增殖,迁移,入侵和EMT.
- 在Wnt/β-catenin通路激活刺激lnc-WAL转录时,观察到一个积极的反循环.
结论:
- lnc-WAL通过稳定Wnt/β-catenin通路,在TNBC恶性进展中发挥主调节作用.
- lnc-WAL在TNBC中起到关键的瘤驱动作用,促进了侵略性的表型.
- lnc-WAL代表了一种有前途的治疗标和TNBC患者的预后生物标志物.
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