ArticleThe Kaohsiung journal of medical sciences2020
Long noncoding RNAs SET-binding factor 2-antisense RNA1 promotes cell growth through targeting miR-431-5p/CDK14 axis in human papillary thyroid cancer.
Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- The Clinical Prognostic Value of lncRNA SBF2-AS1 in Cancer Patients: A Meta-Analysis.Technology in cancer research & treatmentPooled it
- A bioinformatics analysis of the target role of miRNA-431-5p on KLK6 in colorectal cancer.Hereditas · 2025Article
- CircRTN1 acts as a miR-431-5p sponge to promote thyroid cancer progression by upregulating TGFA.Hormones (Athens, Greece) · 2022Article
- Upregulation of FTX expression is associated with a poor prognosis and contributes to the progression of thyroid cancer.Oncology letters · 2021Article
- Emerging roles of a pivotal lncRNA SBF2-AS1 in cancers.Cancer cell international · 2021Review
- LncRNA ABCC6P1 promotes proliferation and migration of papillary thyroid cancer cells via Wnt/β-catenin signaling pathway.Annals of translational medicine · 2021Article
- Long noncoding RNAs SET-binding factor 2-antisense RNA1 promotes cell growth through targeting miR-431-5p/CDK14 axis in human papillary thyroid cancer.The Kaohsiung journal of medical sciences · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
Papillary thyroid cancer (PTC) is a frequent thyroid malignancy. With the significant regulatory role in tumor progression, more attention has been employed to investigate mechanism of long noncoding RNAs (lncRNAs) in progression of PTC. We prospectively explored the mechanism whereby lncRNA SET-binding factor 2-antisense RNA1 (SBF2-AS1) is implicated in pathogenesis of PTC. First, differentially expressed SBF2-AS1 between PTC and normal adjacent thyroid tissues was determined, and result indicated a higher SBF2-AS1 expression in PTC tissues than adjacent normal tissues. Moreover, highly SBF2-AS1 expression predicted a poor prognosis in PTC patients. Second, SBF2-AS1 overexpression promoted cell viability and cycle of PTC, while inhibited cell apoptosis. However, SBF2-AS1 downregulation reduced viability and cycle, while promoted cell apoptosis. Moreover, SBF2-AS1 could bind with miR-431-5p and showed negative correlation with miR-431-5p in PTC patients. Furthermore, miR-431-5p bind with cyclin-dependent kinase (CDK) 14 and showed negative correlation with CDK14 in PTC patients. Finally, overexpression of CDK14 counteracted with the inhibitory role of SBF2-AS1 downregulation on cell viability, cycle, and apoptosis of PTC. In conclusion, SBF2-AS1 exhibited oncogenic property in PTC, and knockdown of SBF2-AS1 could be a therapeutic strategy for PTC.
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