LncRNA PART1 regulates colorectal cancer via targeting miR-150-5p/miR-520h/CTNNB1 and activating Wnt/β-catenin pathway

• DOI: 10.1016/j.biocel.2019.105637
• Publication Date: 2019-10-24T16:20:04Z
• Authors: Taicheng Zhou; Lili Wu; Ning Ma; Fuxin Tang; Zhen Zong; Shuang Chen
• Keywords: Male; 0303 health sciences; RNA, Untranslated; Carcinogenesis; Apoptosis; HCT116 Cells; 3. Good health; Gene Expression Regulation, Neoplastic; Mice; MicroRNAs; 03 medical and health sciences; Animals; Heterografts; Humans; Female; Colorectal Neoplasms; Wnt Signaling Pathway; beta Catenin; Cell Proliferation

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.