LncRNA LINC01503 promotes angiogenesis in colorectal cancer by regulating VEGFA expression via miR-342-3p and HSP60 binding.

IF 2.2 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL Journal of Biomedical Research Pub Date : 2024-10-25 DOI:10.7555/JBR.38.20240190
Dandan Zheng, Xiya Zhang, Jia Xu, Shuwen Chen, Bin Wang, Xiaoqin Yuan
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Abstract

Colorectal cancer (CRC) ranks among the top five most common malignant tumors worldwide and has a high mortality rate. Angiogenesis plays an important role in CRC progression; however, anti-angiogenesis therapy still has many limitations. Long non-coding RNAs (lncRNAs) participate in tumor progression by regulating vascular endothelial growth factor expression in metastatic CRC. Thus, targeting specific lncRNA may provide some new hope for anti-angiogenic strategies. Through analyzing data both from both clinical samples and The Cancer Genome Atlas database, we found that the lncRNA LINC01503 was specifically upregulated in CRC tissues, and was associated with tumor progression and a poor overall survival. We also demonstrated that LINC01503 enhanced the capacity of tube formation and migration of vascular endothelial cells, thus promoting CRC tumorigenesis by upregulating vascular endothelial growth factor A (VEGFA) expression in CRC cells. Mechanistically, LINC01503 promoted the expression of VEGFA by simultaneously regulating the stability of both the mRNA and VEGFA by binding to miR-342-3p and the chaperone HSP60. The upregulation of LINC01503 in CRC cells was attributed to the CREB-binding protein CBP/p300-mediated H3K27 acetylation of the LINC01503 promoter region. Taken together, our findings clarify the mechanism by which LINC01503 may promote CRC angiogenesis, implicating that LINC01503 may serve as a potential prognostic biomarker and therapeutic target for CRC.

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LncRNA LINC01503通过miR-342-3p和HSP60结合调控VEGFA的表达,从而促进结直肠癌的血管生成。
结直肠癌(CRC)是全球最常见的五大恶性肿瘤之一,死亡率很高。血管生成在 CRC 的发展过程中起着重要作用,但抗血管生成疗法仍有许多局限性。长非编码 RNA(lncRNA)通过调节转移性 CRC 中血管内皮生长因子的表达参与肿瘤的进展。因此,靶向特定的lncRNA可能会为抗血管生成策略带来一些新希望。通过分析临床样本和癌症基因组图谱数据库的数据,我们发现lncRNA LINC01503在CRC组织中特异性上调,并与肿瘤进展和总生存率低有关。我们还证实,LINC01503能增强血管内皮细胞的管形成和迁移能力,从而通过上调CRC细胞中血管内皮生长因子A(VEGFA)的表达促进CRC的肿瘤发生。从机理上讲,LINC01503通过与miR-342-3p和伴侣HSP60结合,同时调节mRNA和VEGFA的稳定性,从而促进了VEGFA的表达。LINC01503在CRC细胞中的上调归因于CREB结合蛋白CBP/p300介导的LINC01503启动子区H3K27乙酰化。综上所述,我们的研究结果阐明了LINC01503促进CRC血管生成的机制,表明LINC01503可作为CRC潜在的预后生物标志物和治疗靶点。
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来源期刊
Journal of Biomedical Research
Journal of Biomedical Research MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
4.60
自引率
0.00%
发文量
69
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