Background
LncRNAs play an important regulatory function in the occurrence and progression of papillary thyroid cancer (PTC). This study aimed to investigate the role and mechanism of ATP binding cassette subfamily C member 6 pseudogene 1 (ABCC6P1) in PTC.
Conclusions
Our study confirms that ABCC6P1 exerts an oncogenic activity in PTC which may be mediated by the Wnt/β-catenin pathway, suggesting that ABCC6P1 may be a promising therapeutic target for PTC.
Methods
Cancerous and paracancer normal thyroid tissues were collected from 18 patients with PTC, who were operated at the Second Affiliated Hospital of Harbin Medical University. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to investigate the levels of ABCC6P1. Cell proliferation was evaluated using Cell Counting Kit-8 (CCK-8) and colony formation assays. Wound healing and Transwell invasion assays were performed to examine cell migratory and invasive ability. Western blotting analysis was used to detect the expression levels of EMT-related markers and Wnt/β-catenin signaling pathway-related proteins.
Results
The expression of ABCC6P1 was upregulated in PTC tissues and cells. ABCC6P1 silencing could significantly suppress the proliferation, colony formation ability, migratory and invasive ability in PTC cells. Moreover, knockdown of ABCC6P1 induced cell cycle arrest at G0/G1 phase and inhibited epithelial-mesenchymal transition (EMT) process of PTC cells by increasing the E-cadherin expression, but downregulating N-cadherin and vimentin expression. In addition, knockdown of ABCC6P1 caused a significant decrease in levels of Wnt/β-catenin signaling pathway members (including β-catenin, c-myc, and cyclin D1) in PTC cells. Conclusions: Our study confirms that ABCC6P1 exerts an oncogenic activity in PTC which may be mediated by the Wnt/β-catenin pathway, suggesting that ABCC6P1 may be a promising therapeutic target for PTC.