Journal
ONCOLOGY REPORTS
Volume 45, Issue 4, Pages -Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2021.8001
Keywords
papillary thyroid carcinoma; hsa_circ_0001666; microRNAs; ETS variant transcription factor 4; sponge
Categories
Funding
- Science and Technology Planning Project of Shenyang [19-112-4-013]
- Medical Education Science Research of China Medical University [YDJK2020042]
Ask authors/readers for more resources
The study revealed that upregulated circular RNA hsa_circ_0001666 in papillary thyroid carcinoma (PTC) is associated with lymph node metastasis and promotes cancer aggressiveness. Knocking down hsa_circ_0001666 inhibits cell proliferation and induces apoptosis in PTC. Furthermore, hsa_circ_0001666 promotes PTC tumorigenesis through the miR-330-5p/miR-193a-5p/miR-326/ETV4 pathway, suggesting its potential as a therapeutic target for PTC.
Circular RNAs (circRNAs) are a group of regulators that affect the aggressive behaviors of several types of cancer. Hsa_circ_0001666 (also referred to as hsa_circ_000742) is a newly discovered circRNA that is upregulated in human papillary thyroid carcinoma (PTC) based on microarray analysis. However, the role of hsa_circ_0001666 in PTC progression remains unknown. Thus, the aim of the present study was to determine the potential function and underlying mechanism of hsa_circ_0001666 in PTC. The results demonstrated that hsa_circ_0001666 was upregulated in both PTC clinical samples and cell lines. Its expression was associated with lymph node metastasis of patients with PTC. Knocking down hsa_circ_0001666 expression inhibited cell proliferation, as evidenced by decreased cell viability, arrest of cell cycle progression at the G(1) phase and an increase in cell cycle-associated proteins. Apoptosis rates and expression levels of pro-apoptotic proteins were also increased by silencing hsa_circ_0001666. In xenograft experiments, the oncogenic effect of hsa_circ_0001666 on tumor growth was verified. Additionally, luciferase reporter assays showed that hsa_circ_0001666 and ETS variant transcription factor 4 (ETV4) shared common binding sites with three microRNAs [(miRNA/miR)-330-5p, miR-193a-5p and miR-326]. Knockdown of these miRNAs separately reversed the inhibitory effect of hsa_circ_0001666 small interfering RNAs on PTC tumor aggressiveness, and ETV4 overexpression also induced a similar effect to that of miRNA inhibitors. Thus, hsa_circ_0001666 may function as an oncogene, promoting PTC tumorigenesis via the miR-330-5p/miR-193a-5p/miR-326/ETV4 pathway. This provides a basis for identifying potential novel therapeutic targets for PTC.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available