Open AccessKnockdown of circ_NEK6 Decreased 131I Resistance of Differentiated Thyroid Carcinoma via Regulating miR-370-3p/MYH9 Axis
Author(s) -
Fukun Chen,
Shuting Yin,
Zhiping Feng,
Chao Liu,
Juan Lv,
Yuanjiao Chen,
Ruoxia Shen,
Jiaping Wang,
ZhongLiang Deng
Publication year - 2021
Publication title -
technology in cancer research and treatment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.754
H-Index - 63
eISSN - 1533-0346
pISSN - 1533-0338
DOI - 10.1177/15330338211004950
Subject(s) - gene knockdown , cancer research , apoptosis , radioresistance , chemistry , in vivo , cell growth , thyroid carcinoma , thyroid , microbiology and biotechnology , medicine , biology , radiation therapy , biochemistry
Radioresistance is a crucial factor for the failure of iodine 131 ( 131 I)-based radiotherapy for differentiated thyroid carcinoma (DTC). This study aimed to explore the effect of circ_NEK6 on the development of 131 I resistance in DTC and its potential mechanism. In this study, we demonstrated that circ_NEK6 expression was significantly elevated in 131 I-resistant DTC tissues and cell lines. Knockdown of circ_NEK6 significantly repressed 131 I resistance via inhibiting cell proliferation, migration, invasion abilities, and inducing cell apoptosis and DNA damage in 131 I-resistant DTC cells. Mechanistically, knockdown of circ_NEK6 suppressed 131 I 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 131 I radiation-induced inhibition of xenograft tumor growth. Taken together, knockdown of circ_NEK6 repressed 131 I 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 131 I resistance.