文章：

LOXL1-AS1通过JAK2/STAT3信号通路抑制JAK2泛素化并促进胆管癌进展

LOXL1-AS1 inhibits JAK2 ubiquitination and promotes cholangiocarcinoma progression through JAK2/STAT3 signaling 

原文发布日期：2024-01-24 

英文摘要：

This study thoroughly investigated the role of the long non-coding RNA LOXL1-AS1 in the pathogenesis of cholangiocarcinoma (CCA). Through bioinformatics analysis and tissue samples validation, the study found that LOXL1-AS1 was significantly elevated in CCA, with its high expression closely tied to clinical pathological features and prognosis. In vitro and in vivo experiments revealed that LOXL1-AS1 was crucial in regulating CCA cell apoptosis, proliferation, migration, and invasion. Further investigations using FISH, subcellular localization experiments, RNA pull down, and RIP uncovered that LOXL1-AS1 primarily resided in the cytoplasm and influenced CCA progression by modulating the JAK2/STAT3 signaling pathway. Notably, LOXL1-AS1 might regulate the activity of JAK2 through modulating its ubiquitination and degradation. YY1 had also been found to act as an upstream transcription factor of LOXL1-AS1 to impact CCA cell malignancy. These findings shed light on the pivotal role of LOXL1-AS1 in CCA and offered potential directions for novel therapeutic strategies, providing a fresh perspective on tumor pathogenesis. 

摘要翻译： 

本研究深入探讨了长链非编码RNA LOXL1-AS1在胆管癌（CCA）发病机制中的作用。通过生物信息学分析和组织样本验证，发现LOXL1-AS1在CCA中表达显著升高，其高表达与临床病理特征及预后密切相关。体内外实验表明，LOXL1-AS1在调控CCA细胞凋亡、增殖、迁移和侵袭过程中起关键作用。通过FISH、亚细胞定位实验、RNA pull down及RIP等技术进一步发现，LOXL1-AS1主要定位于细胞质，并通过调控JAK2/STAT3信号通路影响CCA进展。值得注意的是，LOXL1-AS1可能通过调节泛素化降解过程调控JAK2活性。研究还发现YY1作为LOXL1-AS1的上游转录因子影响CCA细胞恶性表型。这些发现揭示了LOXL1-AS1在CCA中的关键作用，为新型治疗策略提供了潜在方向，也为肿瘤发病机制研究提供了新视角。

原文链接：

LOXL1-AS1 inhibits JAK2 ubiquitination and promotes cholangiocarcinoma progression through JAK2/STAT3 signaling