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COL11A1 受 miR-339-5p 下调并促进结肠癌进展。

COL11A1 is Downregulated by miR-339-5p and Promotes Colon Carcinoma Progression.

机构信息

Department of Anorectal Clinic, The Third Affiliated Hospital of LNUTCM, Shenyang, Liaoning 110003, China.

出版信息

Can J Gastroenterol Hepatol. 2022 May 28;2022:8116990. doi: 10.1155/2022/8116990. eCollection 2022.

Abstract

The roles of COL11A1 in cancer have been increasingly considered, but the understandings of the effects of COL11A1 on colon carcinoma progress are much limited yet. qRT-PCR and Western blot were utilized to evaluate COL11A1 expression at mRNA and protein levels, respectively, in colon carcinoma cell lines. Afterward, the tumorigenesis biological effects of COL11A1 were examined by CCK-8, colony formation, Transwell, and wound healing methods. Moreover, upstream miRNAs containing the binding sites with COL11A1 were predicted by the bioinformatics methods. The interplay between COL11A1 and miR-339-5p was identified by a dual-luciferase assay. COL11A1 expression was prominently upregulated in colon carcinoma cell lines relative to that in normal human colon mucosal epithelial cell lines, and it was related to tumor stages. The outcomes of experiments suggested that interfering with COL11A1 remarkably repressed the malignant behaviors of SW480 and SW620 cells. MiR-339-5p was markedly lowly expressed in colon carcinoma cell lines. Furthermore, miR-339-5p directly targeted and negatively regulated COL11A1 expression. COL11A1 upregulation promoted colon carcinoma cell functions, while overexpressing miR-339-5p evidently attenuated the promotion. These results proved the modulation of the miR-339-5p/COL11A1 axis in colon carcinoma cells, and miR-339-5p repressed colon carcinoma progression via COL11A1 downregulation. These results offer new underlying targets for the accurate therapy of colon carcinoma patients.

摘要

COL11A1 在癌症中的作用已越来越受到关注,但人们对 COL11A1 对结肠癌进展影响的认识还很有限。我们分别采用 qRT-PCR 和 Western blot 检测了结肠癌细胞系中 COL11A1 的 mRNA 和蛋白水平表达。随后,通过 CCK-8、集落形成、Transwell 和划痕愈合实验检测了 COL11A1 的肿瘤发生生物学效应。此外,还通过生物信息学方法预测了包含 COL11A1 结合位点的上游 miRNA。通过双荧光素酶报告基因实验鉴定了 COL11A1 和 miR-339-5p 之间的相互作用。COL11A1 在结肠癌细胞系中的表达明显高于正常人类结肠黏膜上皮细胞系,且与肿瘤分期有关。实验结果表明,干扰 COL11A1 可显著抑制 SW480 和 SW620 细胞的恶性行为。miR-339-5p 在结肠癌细胞系中表达明显下调。此外,miR-339-5p 可直接靶向并负调控 COL11A1 的表达。COL11A1 的上调促进了结肠癌细胞的功能,而过表达 miR-339-5p 则明显减弱了这种促进作用。这些结果证明了 miR-339-5p/COL11A1 轴在结肠癌细胞中的调控作用,以及 miR-339-5p 通过下调 COL11A1 抑制结肠癌的进展。这些结果为结肠癌患者的精准治疗提供了新的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b515/9167123/022ea03d51d9/CJGH2022-8116990.001.jpg

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