| Literature DB >> 33759638 |
Fukun Chen1, Shuting Yin2, Zhiping Feng1, Chao Liu1, Juan Lv1, Yuanjiao Chen1, Ruoxia Shen1, Jiaping Wang3, Zhiyong Deng1.
Abstract
Radioresistance is a crucial factor for the failure of iodine 131 (131I)-based radiotherapy for differentiated thyroid carcinoma (DTC). This study aimed to explore the effect of circ_NEK6 on the development of 131I resistance in DTC and its potential mechanism. In this study, we demonstrated that circ_NEK6 expression was significantly elevated in 131I-resistant DTC tissues and cell lines. Knockdown of circ_NEK6 significantly repressed 131I resistance via inhibiting cell proliferation, migration, invasion abilities, and inducing cell apoptosis and DNA damage in 131I-resistant DTC cells. Mechanistically, knockdown of circ_NEK6 suppressed 131I resistance in DTC by upregulating the inhibitory effect of miR-370-3p on the expression of myosin heavy chain 9 (MYH9). In vivo experiments showed that circ_NEK6 inhibition aggravated 131I radiation-induced inhibition of xenograft tumor growth. Taken together, knockdown of circ_NEK6 repressed 131I resistance in DTC cells by regulating the miR-370-3p/MYH9 axis, indicating that circ_NEK6 may act as a potential biomarker and therapeutic target for DTC patients with 131I resistance.Entities:
Keywords: MYH9; circ_NEK6; differentiated thyroid carcinoma; iodine 131; malignant biological behavior; miR-370-3p
Year: 2021 PMID: 33759638 DOI: 10.1177/15330338211004950
Source DB: PubMed Journal: Technol Cancer Res Treat ISSN: 1533-0338