| Literature DB >> 33604734 |
Chongwen Xu1, Yuan Shao1, Junsong Liu1, Xiaobao Yao1, Fang Quan1, Qian Zhao1, Ruimin Zhao1, Bo Kou1, Honghui Li1, Peng Han1, Xuan Wang1, Yanxia Bai1, Zhiwei Zheng2, Shaoqiang Zhang3.
Abstract
Long non-coding RNA (lncRNA) AGAP2-AS1 acts as an oncogene in several types of cancers. However, the role and mechanism of AGAP2-AS1 in papillary thyroid carcinoma (PTC) remain unclear. Thus, in this study, we aimed to explore the role of AGAP2-AS1 in PTC. Our results showed that AGAP2-AS1 was significantly upregulated in PTC tissues. Knockdown of AGAP2-AS1 inhibited the proliferation, migration and invasion of PTC cells. In vivo experiment showed that AGAP2-AS1 knockdown inhibited the tumorigenesis of PTC. MiR-628-5p was found to act as a target miRNA of AGAP2-AS1 in PTC. The expression level of miR-628-5p in PTC tissues was negatively associated with that of AGAP2-AS1. Inhibition of miR-628-5p attenuated the effects of AGAP2-AS1 knockdown on PTC. Moreover, miR-628-5p directly bound to the 3'UTR of KLF12 and inhibited the expression of KLF12. Knockdown of KLF12 enhanced the inhibitory effects of miR-628-5p on PTC cell proliferation and metastasis. In conclusion, these findings indicated that AGAP2-AS1 exerted an oncogenic role in PTC progression and metastasis. The effects of AGAP2-AS1 might be mediated by the regulation of miR-628-5p/KLF12 axis.Entities:
Keywords: AGAP2-AS1; KLF12; Long non‐coding RNA (lncRNA); Metastasis; Papillary thyroid carcinoma (PTC); miR-628-5p
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Year: 2021 PMID： 33604734 DOI： 10.1007/s10863-021-09879-3
Source DB: PubMed Journal: J Bioenerg Biomembr ISSN： 0145-479X Impact factor: 2.945