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LINC01836 Promotes Colorectal Cancer Progression and Functions as ceRNA to Target SLC17A9 by Sponging miR-1226-3p
Protein & Peptide Letters ( IF 1.6 ) Pub Date : 2023-12-06 , DOI: 10.2174/0109298665248028231122064831
Zhihua Xu 1 , Yue Yu 1 , Hao Ni 2 , Wei Sun 3 , Yuting Kuang 1
Affiliation  

Background: Increasing evidence proves that long non-coding RNAs (lncRNAs) play a key role in the occurrence and development of colorectal cancer. However, the function and molecular mechanism of LINC01836 in CRC are still unknown. Methods: The differentially expressed lncRNAs in colorectal cancer were obtained from the RNA sequencing data. The effects of LINC01836 on colorectal cancer cells were tested in in vitro experiments. The mechanism of LINC01836 action was investigated through western blot, RNA immunoprecipitation assay and luciferase reporter assay. Moreover, the xenograft mouse model was conducted to examine the effects of LINC01836 in vivo. Results: In this study, we showed that LINC01836 was significantly elevated in colorectal cancer tissues and cells. Elevated LINC01836 expression significantly correlated with larger tumor size, positive lymph node metastasis, distant metastasis, advanced tumor-node-metastasis (TNM) stage, and poor prognosis. Furthermore, decreased expression of LINC01836 repressed proliferation, migration, and invasion in vitro and vivo, and high LINC01836 expression displayed the opposite effect. Further analysis revealed that LINC01836 could regulate the expression of SLC17A9 by competing with miR-­‐1226-3p. Furthermore, down-regulation of LINC01836 or increased expression of miR-­‐1226-3p markedly reversed the effects of SLC17A9 overexpression on colorectal cancer cells. Conclusion: This study showed that LINC01836 regulated the expression of SLC17A9 through sponge miR-1226-3p by acting as a competitive endogenous RNA (ceRNA), promoted the progression of colorectal cancer, and suggested a new prognostic biomarker and potential cancer treatment target for colorectal cancer.

中文翻译:

LINC01836 通过海绵 miR-1226-3p 促进结直肠癌进展并作为 ceRNA 靶向 SLC17A9

背景:越来越多的证据证明长链非编码RNA(lncRNA)在结直肠癌的发生和发展中发挥着关键作用。然而,LINC01836在CRC中的功能和分子机制仍不清楚。方法:从RNA测序数据中获取结直肠癌中差异表达的lncRNA。在体外实验中测试了LINC01836对结直肠癌细胞的影响。通过蛋白质印迹、RNA 免疫沉淀测定和荧光素酶报告基因测定研究了 LINC01836 的作用机制。此外,还建立了异种移植小鼠模型来检查LINC01836的体内作用。结果:在这项研究中,我们发现 LINC01836 在结直肠癌组织和细胞中显着升高。LINC01836 表达升高与肿瘤体积较大、淋巴结转移阳性、远处转移、晚期肿瘤淋巴结转移 (TNM) 分期和不良预后显着相关。此外,LINC01836的表达减少会抑制体外和体内的增殖、迁移和侵袭,而LINC01836的高表达则表现出相反的效果。进一步分析表明,LINC01836可以通过与miR-‐1226-3p竞争来调节SLC17A9的表达。此外,LINC01836 的下调或 miR-1226-3p 表达的增加显着逆转了 SLC17A9 过表达对结直肠癌细胞的影响。结论:本研究表明LINC01836通过海绵miR-1226-3p作为竞争性内源RNA(ceRNA)调节SLC17A9的表达,促进结直肠癌的进展,为结直肠癌提出了一个新的预后生物标志物和潜在的癌症治疗靶点。癌症。
更新日期:2023-12-06
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