ArticleAnnals of translational medicine2021
LncRNA ABCC6P1 promotes proliferation and migration of papillary thyroid cancer cells via Wnt/β-catenin signaling pathway.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- C-MYC as a key effector of WNT, PI3K/AKT, MAPK, and TGF-β signaling pathways in regulation of epithelial-mesenchymal transition during tumor metastasis.Cancer cell international · 2026Review
- Dual roles of long non-coding RNAs in thyroid cancer: regulation of programmed cell death pathways.Medical oncology (Northwood, London, England) · 2025Review
- PTEN inhibits epithelial mesenchymal transition of thyroid cancer cells by regulating the Wnt/β-Catenin signaling pathway.Discover oncology · 2024Article
- Diagnostic Value of Plasma Long Non-coding SLC26A4 Antisense RNA 1 Combined with Magnetic Resonance Imaging in Rectal Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024Article
- Purinergic signaling in thyroid disease.Purinergic signalling · 2023Review
- Overexpression of ST7-AS1 Enhances Apoptosis and Inhibits Proliferation of Papillary Thyroid Carcinoma Cells Via microRNA-181b-5p-Dependent Inhibition Tripartite Motif Containing 3.Molecular biotechnology · 2023Article
- Roles, molecular mechanisms, and signaling pathways of TMEMs in neurological diseases.American journal of translational research · 2021Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLncRNAs 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.
methodsCancerous 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.
resultsThe 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.
conclusionsOur 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.
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