Numerous studies have reported that lncRNAs could play a significant role in carcinogenesis. PART1, as an identified lncRNA, was an oncogene in several cancers. However, the underling mechanism of PART1 regulating colorectal cancer remains unknown. qRT-PCR was used to measure relevant RNAs expression. CCK8 and colony formation were combined to evaluate cell proliferation. Tunel and flow cytometry were performed to access cell apoptosis. Wound healing and Transwell assay testified cell invasion and migration ability. Relevant protein expression level was measured via Western blot assay. TOP/FOP luciferase assay determined the activity of Wnt/β-catenin pathway. According to experiment findings, PART1 was up-regulated in CRC tissues and cell lines. Inhibition of PART1 hindered CRC cell proliferation, invasion and migration, while promoting CRC cell apoptosis. Experiments in vivo also validated this result. Mechanistically, PART1 sponged miR-150-5p/miR-520 h to up-regulate CTNNB1, thus activating Wnt/β-catenin pathway in CRC. In summary, PART1 could up-regulate CTNNB1 via sponging miR-150-5p/miR-520 h.

大量研究报告称，lncRNA在癌变过程中可能起重要作用。作为鉴定出的lncRNA，PART1是几种癌症中的癌基因。然而，PART1调节结直肠癌的基本机制仍然未知。使用qRT-PCR测量相关的RNA表达。CCK8和集落形成相结合以评估细胞增殖。进行Tunel和流式细胞术以进入细胞凋亡。伤口愈合和Transwell分析证实了细胞的侵袭和迁移能力。通过蛋白质印迹测定法测量相关的蛋白质表达水平。TOP / FOP荧光素酶测定确定了Wnt /β-catenin途径的活性。根据实验结果，PART1在CRC组织和细胞系中上调。抑制PART1会阻止CRC细胞增殖，侵袭和迁移，同时促进CRC细胞凋亡。体内实验也验证了这一结果。机械上，PART1使miR-150-5p / miR-520h上调CTNNB1，从而激活CRC中的Wnt /β-catenin途径。总而言之，PART1可以通过使miR-150-5p / miR-520h变海绵来上调CTNNB1。