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- Title
Long non-coding RNA AFAP1-AS1 promotes thyroid cancer progression by sponging miR-204-3p and upregulating DUSP4.
- Authors
Ma, Hongzhi; Shi, Qian; Fang, Jugao; Wang, Ru; Zhao, Jianyu; Lin, Sitong; Dong, Jiajing; Zhang, Yan; Shen, Xixi; Chen, Jiaming; Zhong, Qi
- Abstract
Long non-coding RNA actin filament-associated protein 1-antisense RNA 1 (AFAP1-AS1) shows crucial regulatory function in tumor progression. Nonetheless, the biological function and underlying mechanism of AFAP1-AS1 in the progression of thyroid cancer is still unclear. Expressions of AFAP1-AS1, miR-204-3p and DUSP4 were quantified utilizing quantitative real-time polymerase chain reaction and/or western blot. In loss-of-function and gain-of-function assays, cell proliferation, migration and invasion were appraised by CCK-8 assay, wound healing assay, Transwell migration and invasion assays, respectively. Luciferase reporter assay was employed for validating the interaction between miR-204-3p and AFAP1-AS1 or the 3'UTR of dual specificity phosphatase 4 (DUSP4). AFAP1-AS1 was highly expressed in thyroid cancer tissues and cell lines. Highly expressed AFAP1-AS1 was in association with advanced TNM stage and positive lymph node metastasis. Knockdown of AFAP1-AS1 suppressed the proliferation, migration and invasion of thyroid cancer cells, and overexpression of AFAP1-AS1 induced a reversed effect. MiR-204-3p was targetedly repressed by AFAP1-AS1, and miR-204-3p could negatively regulate DUSP4 expression. AFAP1-AS1 augmented the expression of DUSP4 via repressing miR-204-3p, and the effects of AFAP1-AS1 overexpression on thyroid cancer cells were also partly abolished by miR-204-3p restoration. In summary, AFAP1-AS1 facilitates thyroid cancer cell proliferation, migration and invasion by regulating miR-204-3p/DUSP4 axis.
- Subjects
LINCRNA; THYROID cancer; NON-coding RNA; CANCER invasiveness; CANCER cell proliferation; LYMPHATIC metastasis; THYROID gland
- Publication
Journal of Biochemistry, 2022, Vol 171, Issue 1, p131
- ISSN
0021-924X
- Publication type
Article
- DOI
10.1093/jb/mvab109