Mesh : Carcinoma Cell Line, Tumor Cell Proliferation / genetics Collagen Type XI Colonic Neoplasms / genetics pathology Humans MicroRNAs / genetics metabolism

来  源:   DOI:10.1155/2022/8116990   PDF(Pubmed)

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 in-vitro 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在癌症中的作用已被越来越多地考虑,但是对COL11A1对结肠癌进展的影响的理解还很有限。qRT-PCR和Westernblot用于评估COL11A1在mRNA和蛋白质水平的表达,分别,在结肠癌细胞系中。之后,通过CCK-8、集落形成、Transwell,和伤口愈合方法。此外,通过生物信息学方法预测含有与COL11A1结合位点的上游miRNA。通过双荧光素酶测定鉴定COL11A1和miR-339-5p之间的相互作用。与正常人结肠粘膜上皮细胞系相比,结肠癌细胞系中的COL11A1表达明显上调,和肿瘤分期有关.体外实验结果表明,干扰COL11A1可显着抑制SW480和SW620细胞的恶性行为。MiR-339-5p在结肠癌细胞系中明显低表达。此外,miR-339-5p直接靶向并负调控COL11A1表达。COL11A1上调促进结肠癌细胞功能,而过表达miR-339-5p的作用明显减弱。这些结果证明了miR-339-5p/COL11A1轴在结肠癌细胞中的调节,miR-339-5p通过COL11A1下调抑制结肠癌的进展。这些结果为结肠癌患者的准确治疗提供了新的潜在目标。
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