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LOC344887通过调节SHP1调控的STAT3/HMGA2信号轴在促进肝细胞癌进展中的新作用。

The novel role of LOC344887 in the enhancement of hepatocellular carcinoma progression via modulation of SHP1-regulated STAT3/HMGA2 signaling axis.

作者信息

Lin Yang-Hsiang, Chi Hsiang-Cheng, Wu Meng-Han, Liao Chia-Jung, Chen Cheng-Yi, Huang Po-Shuan, Huang Wei-Chieh, Wang Yi-Wen, Lin Tzu-Kang, Lai Ming-Wei, Yeh Chau-Ting, Lin Kwang-Huei

机构信息

Liver Research Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan.

Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan.

出版信息

Int J Biol Sci. 2024 Dec 2;20(15):6281-6296. doi: 10.7150/ijbs.99683. eCollection 2024.

Abstract

Pseudogene-derived long non-coding RNAs (lncRNAs) have become crucial regulators in cancer progression. Extensive research highlights the pivotal role of signal transducer and activator of transcription 3 (STAT3) in promoting hepatocellular carcinoma (HCC) progression. As a result, targeting aberrant STAT3 activation presents a promising therapeutic strategy for HCC. Our study aims to identify the key pseudogene-derived lncRNA involved in modulating STAT3 activation and driving HCC progression. Our study is the first to identify a significant upregulation of LOC344887, a pseudogene-derived lncRNA, in HCC tissues. Elevated LOC344887 levels correlated with poor overall survival (OS) and recurrence-free survival (RFS), highlighting its potential as a biomarker for HCC. The rapid amplification of cDNA ends (RACE) and RT-PCR experiments revealed the expression of a novel LOC344887 transcript, named LOC344887-v2, alongside the annotated RefSeq transcript NR_151491 (LOC344887-v1) in both HCC tissues and hepatoma cell lines. Functional assays demonstrated that LOC344887 enhances cellular migration and invasion, with its variant LOC344887-v2 exhibiting a more pronounced effect. Further, LOC344887 mechanistically regulates STAT3 phosphorylation at tyrosine 705, which is crucial for maintaining STAT3 activation in HCC. Our findings unravel that LOC344887 not only physically interacts with p-STAT3 but also prevents its dephosphorylation by src homology region 2 domain-containing phosphatase 1 (SHP-1), thereby sustaining oncogenic signaling. In addition, we identified HMGA2 as a target of the LOC344887/SHP-1/STAT3 axis, with higher HMGA2 expression correlating with poorer prognosis in HCC patients. The ability of LOC344887 to regulate HMGA2 through direct binding of STAT3 to its promoter underlines its role in HCC progression. Collectively, these findings elucidate a novel oncogenic role of LOC344887 in HCC and suggest that targeting this lncRNA and its associated pathways may provide novel therapeutic strategies for improving patient outcomes in HCC.

摘要

假基因衍生的长链非编码RNA(lncRNAs)已成为癌症进展中的关键调节因子。广泛的研究突出了信号转导和转录激活因子3(STAT3)在促进肝细胞癌(HCC)进展中的关键作用。因此,靶向异常的STAT3激活为HCC提供了一种有前景的治疗策略。我们的研究旨在确定参与调节STAT3激活和推动HCC进展的关键假基因衍生lncRNA。我们的研究首次发现假基因衍生的lncRNA LOC344887在HCC组织中显著上调。LOC344887水平升高与总生存期(OS)和无复发生存期(RFS)较差相关,突出了其作为HCC生物标志物的潜力。cDNA末端快速扩增(RACE)和RT-PCR实验揭示了一种新的LOC344887转录本,命名为LOC344887-v2,在HCC组织和肝癌细胞系中与注释的RefSeq转录本NR_151491(LOC344887-v1)一起表达。功能分析表明,LOC344887增强细胞迁移和侵袭,其变体LOC344887-v2表现出更显著的作用。此外,LOC344887在机制上调节STAT3酪氨酸705位点的磷酸化,这对于维持HCC中STAT3的激活至关重要。我们的研究结果表明,LOC344887不仅与p-STAT3发生物理相互作用,还通过含src同源区2结构域的磷酸酶1(SHP-1)阻止其去磷酸化,从而维持致癌信号。此外,我们确定HMGA2是LOC344887/SHP-1/STAT3轴的靶点,HCC患者中较高的HMGA2表达与较差的预后相关。LOC344887通过STAT3直接结合其启动子来调节HMGA2的能力强调了其在HCC进展中的作用。总的来说,这些发现阐明了LOC344887在HCC中的一种新的致癌作用,并表明靶向这种lncRNA及其相关途径可能为改善HCC患者的预后提供新的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60b6/11628343/1ffd5cea8bda/ijbsv20p6281g001.jpg

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