Long non-coding RNA AFAP1-AS1 promotes thyroid cancer progression by sponging miR-204-3p and upregulating DUSP4

Abstract

Long non-coding RNA (lncRNA) 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 qRT-PCR 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.

Exosomal AFAP1-AS1 promotes the growth, metastasis, and glycolysis of pituitary adenoma by preventing HuR degradation

“…[15] Numerous studies have also shown that AFAP1-AS1 is often dysregulated in various human cancers, including thyroid, lung, and breast cancer, as well as osteosarcoma and PA, and its aberrant expression regulates numerous hallmarks to promote tumor development, invasion, and metastasis, such as proliferation, apoptosis, metastasis, and glycolysis. [12,13,[23][24][25][26] In PA, downregulation of AFAP1-AS1 impeded cell proliferation, growth hormone and prolactin secretion, and induced cell apoptosis and G/S cell cycle arrest. [13] In the present study, we found that AFAP1-AS1 was signi cantly upregulated in cells treated with exosomes derived from PA.…”

Elevated LINC00894 relieves the oncogenic properties of thyroid cancer cell by sponging let-7e-5p to promote TIA-1 expression

“…lncRNAs play a regulatory role in tumors by functioning as miRNA sponges to competitively regulate the miRNA-targeted genes, also known as the competing endogenous RNA (ceRNA) mechanism. In thyroid cancer, AFAP1-AS1, TNRC6C-AS1, and LINC00284 regulate cancer occurrence and progression by sponging miR-204-3p, miR-513c-5p, and miR-30d-5p, respectively [ 13 – 15 ]. LINC00894 can sponge miR-429 to promote the progression of breast cancer [ 11 ].…”