Long intergenic non-protein-coding RNA 467 promotes tumor progression and angiogenesis via the microRNA-128-3p/vascular endothelial growth factor C axis in colorectal cancer.
Long intergenic non-protein-coding RNA 467 promotes tumor progression and angiogenesis via the microRNA-128-3p/vascular endothelial growth factor C axis in colorectal cancer.
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DOI：
10.1080/21655979.2022.2074666
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发表时间：
2022-05
期刊：
影响因子：
4.9
通讯作者：
中科院分区：
文献类型：
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作者：
长链非编码rna （lncRNAs）是肿瘤发生和转移的重要调控因子和生物标志物。长基因间非蛋白编码RNA 467 （LINC00467）与多种癌症相关。然而，人们对LINC00467在结直肠癌（CRC）促进中的作用和机制知之甚少。本研究旨在揭示LINC00467在结直肠癌进展中的新细节。逆转录-聚合酶链反应表明，LINC00467在结直肠癌组织和细胞系中的表达水平显著上调，这与结直肠癌的临床特征密切相关。细胞和动物研究表明，下调CRC细胞中LINC00467的表达可显著抑制细胞增殖、转移和血管生成。此外，LINC00467的过表达加速了CRC的促进。生物信息学分析和荧光素酶报告基因检测证实LINC00467与miR-128-3p结合。挽救实验表明，miR-128-3p水平降低可以通过沉默LINC00467逆转CRC细胞抑制。此外，血管内皮生长因子C （VEGFC）被确定为miR-128-3p的靶标，可以逆转miR-128-3p介导的细胞生长抑制。总之，我们的研究结果表明，LINC00467通过miR-128-3p/VEGFC轴促进结直肠癌的进展和血管生成。我们的发现扩大了对结直肠癌机制的理解，并提出了针对结直肠癌的临床策略的潜在目标。
Long non-coding RNAs (lncRNAs) are important regulators and biomarkers of tumorigenesis and tumor metastasis. Long intergenic non-protein-coding RNA 467 (LINC00467) is associated with various cancers. However, the role and mechanism of LINC00467 in colorectal cancer (CRC) promotion are poorly understood. This study aimed to present new details of LINC00467 in the progression of CRC. Reverse transcription–polymerase chain reaction demonstrated that the expression level of LINC00467 in CRC tissues and cell lines was significantly upregulated, which was closely related to the clinical features of CRC. Cell and animal studies showed that the downregulation of LINC00467 expression in CRC cells significantly inhibited cell proliferation, metastasis, and angiogenesis. Moreover, the overexpression of LINC00467 accelerated CRC promotion. Bioinformatics analysis and luciferase reporter assay confirmed that LINC00467 binds to miR-128-3p. Rescue experiments manifested that decreased miR-128-3p level reversed CRC cell inhibition by silencing LINC00467. Furthermore, vascular endothelial growth factor C (VEGFC) was identified as a target of miR-128-3p that could reverse the inhibition of cell growth that is mediated by miR-128-3p. Altogether, our results showed that LINC00467 contributes to CRC progression and angiogenesis via the miR-128-3p/VEGFC axis. Our findings expand the understanding of the mechanisms underlying CRC and suggest potential targets for clinical strategies against CRC.
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DOI：
10.1186/s10020-020-00222-x
发表时间：
2021-02-01
期刊：
Molecular medicine (Cambridge, Mass.)
影响因子：
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作者：
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通讯作者：
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