MicroRNA‑744 suppresses cell proliferation and invasion of papillary thyroid cancer by directly targeting NOB1 Retraction in /10.3892/mmr.2023.13066

Liu,Haixia; Guo,Jing; Chai,Hongyan; Meng,Xiangfeng

doi:10.3892/mmr.2019.9826

MicroRNA‑744 suppresses cell proliferation and invasion of papillary thyroid cancer by directly targeting NOB1

Retraction in: /10.3892/mmr.2023.13066

Authors:
- Haixia Liu
- Jing Guo
- Hongyan Chai
- Xiangfeng Meng
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Affiliations: Department of General Surgery, Weifang People's Hospital, Weifang, Shandong 261041, P.R. China, Department of General Surgery, Yiyuan County People's Hospital, Zibo, Shandong 256199, P.R. China
Published online on: January 4, 2019 https://doi.org/10.3892/mmr.2019.9826
Pages: 1903-1910

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Abstract

MicroRNAs (miRs) serve important roles in the formation and progression of papillary thyroid cancer (PTC) by regulating numerous physiological and pathological behaviours. Thus, investigating the functional roles of specific miRNAs in PTC may contribute in identifying effective therapeutic targets for the management of patients with PTC. miR‑744 is emerging as a cancer‑associated miRNA in numerous types of human cancers; however, the expression and specific functions of miR‑744 in PTC are yet to be determined, and the mechanism underlying the regulatory roles of miR‑744 in PTC remains unknown. In the present study, miR‑744 expression was significantly decreased in PTC tissues and cell lines, as detected by reverse transcription‑quantitative polymerase chain reaction. miR‑744 restoration inhibited cell proliferation and invasion in PTC. Bioinformatics analysis predicted NIN1 (RPN12) binding protein 1 homolog (NOB1) as a potential target of miR‑744. Subsequent experiments validated NOB1 as a direct target gene of miR‑744 in PTC. Furthermore, NOB1 was upregulated in PTC tissues and negatively correlated with miR‑744 expression. NOB1 overexpression could counteract miR‑744‑mediated antitumor effects on PTC cells. In summary, these findings indicated that miR‑744 may inhibit the progression of PTC by directly targeting NOB1. The identification of the miR‑744/NOB1 axis may provide insight into potential targets for the treatment of patients with PTC and improve their prognosis.

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