LSM12在葡萄膜黑色素瘤肿瘤发生中的功能特征

IF 3.4
Junjie Tang , Fengyu Sun , Yi Ren , Liling Chen , Yang Gao , Jinmiao Li , Yaoming Liu , Chao Cheng , Ping Zhang , Shuxia Chen , Siming Ai , Yuxiang Mao , Shicai Su , Rong Lu
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引用次数: 0

摘要

目的本研究旨在探讨LSM12在葡萄膜黑色素瘤(UM)肿瘤发生和进展中的作用,研究其作为预后生物标志物和治疗靶点的潜力。方法分析slsm12在UM中表达与RNA修饰基因和肿瘤干性的关系。使用siRNA敲除UM细胞系的LSM12,然后进行细胞活力和迁移试验。使用皮下异种移植模型评估靶向LSM12的治疗潜力。此外,我们还探讨了LSM12与PI3K/Akt/mTOR通路的关系。结果slsm12在UM患者中表达水平显著升高,与预后不良密切相关。LSM12的表达与RNA甲基化修饰和癌症干细胞特征相关的多个基因呈正相关。LSM12的敲低有效地破坏了UM细胞的体外活力和迁移,并抑制了OCM1异种移植物的体内生长。此外,LSM12敲低导致PI3K/Akt/mTOR通路在体内和体外均受到显著抑制。结论LSM12表达升高与UM的不良预后相关,并在很大程度上促进了肿瘤发生过程,包括肿瘤细胞活力、迁移和肿瘤发生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Functional characterization of LSM12 as a driver in uveal melanoma oncogenesis

Objective

This study aimed to investigate the role of LSM12 in uveal melanoma (UM) oncogenesis and progression, examining its potential as both a prognostic biomarker and therapeutic target.

Methods

LSM12 expression was analyzed in relation to RNA modification genes and tumor stemness in UM. UM cell lines were subjected to LSM12 knockdown using siRNA, followed by cell viability and migration assays. The therapeutic potential of targeting LSM12 was evaluated using a subcutaneous xenograft model. Additionally, the relationship between LSM12 and the PI3K/Akt/mTOR pathway was explored.

Results

LSM12 expression levels were significantly elevated in UM patients, correlating strongly with poor prognosis. Positive correlations were observed between LSM12 expression and multiple genes associated with RNA methylation modifications and cancer stem cell characteristics. Knockdown of LSM12 effectively disrupted UM cell viability and migration in vitro and inhibited OCM1 xenograft growth in vivo. Additionally, LSM12 knockdown resulted in notable inhibition of the PI3K/Akt/mTOR pathway both in vitro and in vivo.

Conclusions

Elevated LSM12 expression correlates with poor prognosis in UM and critically promotes oncogenic processes, including tumor cell viability, migration, and tumorigenesis.
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来源期刊
CiteScore
1.70
自引率
0.00%
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审稿时长
66 days
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