长非编码RNA LGALS8-AS1促进非小细胞肺癌癌症的血管生成和脑转移。

IF 1.4 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Acta biochimica Polonica Pub Date : 2023-09-16 DOI:10.18388/abp.2020_6501
Jian Zhong, Bo Wang
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引用次数: 0

摘要

脑转移(BM)与癌症(NSCLC)患者预后不良有关。考虑到这一点,LGAS8-AS1介导的BM进展在NSCLC中进行了探讨。分析了60例NSCLC患者(30例无骨髓,30例有骨髓)的临床特点。患有BM的NSCLC患者的LGALS8-AS1水平高于没有BM的NSCLC.消耗LGALS8-AS1在体外阻止NSCLC细胞增殖、迁移、侵袭和血管生成,在体内阻止NSCLC肿瘤发生和BM。LGALS8-AS1靶向miR-885-3p介导Fascin-actin-bundling protein 1(FSCN1)的表达。恢复miR-885-3p抑制了NSCLC的生长、血管生成和BM,FSCN1诱导挽救了LGALS8-AS1缺失对NSCLC细胞的表现。我们的研究结果为LGALS8-AS1介导的NSCLC转移提供了新的见解,并表明LGALS8-AS1可能是鉴定具有转移潜力的NSCLC的有用生物标志物。
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Long noncoding RNA LGALS8-AS1 promotes angiogenesis and brain metastases in non-small cell lung cancer.

Brain metastases (BM) are associated with poor prognosis in patients with non-small cell lung cancer (NSCLC). Considering that, LGAS8-AS1-mediated progression of BM was probed in NSCLC. The clinical characteristics of 60 NSCLC patients (30 without BM and 30 with BM) were analyzed. NSCLC patients with BM had higher levels of LGALS8-AS1 than NSCLC patients without BM. Depleting LGALS8-AS1 prevented NSCLC cell proliferation, migration, invasion, and angiogenesis in vitro, and NSCLC tumorigenesis and BM in vivo. LGALS8-AS1 targeted miR-885-3p to mediate Fascin actin-bundling protein 1 (FSCN1) expression. Restoring miR-885-3p inhibited NSCLC growth, angiogenesis, and BM, and FSCN1 induction rescued the performance of LGALS8-AS1 depletion on NSCLC cells. Our results provide new insights into LGALS8-AS1-mediated NSCLC metastasis and suggest that LGALS8-AS1 may be a useful biomarker for identifying NSCLC with metastatic potential.

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来源期刊
Acta biochimica Polonica
Acta biochimica Polonica 生物-生化与分子生物学
CiteScore
2.40
自引率
0.00%
发文量
99
审稿时长
4-8 weeks
期刊介绍: Acta Biochimica Polonica is a journal covering enzymology and metabolism, membranes and bioenergetics, gene structure and expression, protein, nucleic acid and carbohydrate structure and metabolism.
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