Author/Authors :
Fan, Yaohua Department of Oncology - The Second Affiliated Hospital of Jiaxing University - Jiaxing - Zhejiang Province, China , Fei, MingJian Department of Pathology - The Second Affiliated Hospital of Jiaxing University - Jiaxing - Zhejiang Province, China , Li, Yan Department of Oncology - The Second Affiliated Hospital of Jiaxing University - Jiaxing - Zhejiang Province, China , Gao, Zhenzhen Department of Oncology - The Second Affiliated Hospital of Jiaxing University - Jiaxing - Zhejiang Province, China , Zhu, Yuzhang Department of Oncology - The Second Affiliated Hospital of Jiaxing University - Jiaxing - Zhejiang Province, China , Dai, Guiping Department of Oncology - The Second Affiliated Hospital of Jiaxing University - Jiaxing - Zhejiang Province, China , Wu, Dongjuan Department of Oncology - The Second Affiliated Hospital of Jiaxing University - Jiaxing - Zhejiang Province, China
Abstract :
Thyroid cancer (TC) is the most common endocrine malignant disease with a rising morbidity year by year. Accumulating studies
have shown that microRNAs (miRNAs) play a regulatory role in the progression of various tumors, but the molecular regulatory
mechanism of miR-196a-2 in TC is still unknown. qRT-PCR was employed to measure the expression of miR-196a-2 and NRXN1
mRNA in TC cells, while western blot was used to detect the protein expression of NRXN1. CCK-8, colony formation and flow
cytometry assays were used to measure cell proliferation and apoptosis of TC cells. Dual-luciferase reporter gene assay was used
to predict and verify the targeted binding relationship between miR-196a-2 and NRXN1. Our study results manifested that miR196a-2 was dramatically overexpressed in cells of TC, while NRXN1 was lowly expressed. miR-196a-2 could promote cell
proliferation and inhibit cell apoptosis of TC. Additionally, miR-196a-2 could also target and inhibit the expression of NRXN1.
Silencing NRXN1 could reverse the inhibitory effect of miR-196a-2 downregulation on cell proliferation of TC, as well as the
promoting effect on cell apoptosis. In a conclusion, we found that miR-196a-2 could promote cell proliferation and inhibit cell
apoptosis of TC by targeting NRXN1. Therefore, miR-196a-2/NRXN1 is potential to be a molecular therapeutic target for TC.
Keywords :
NRXN1 , Thyroid , miR-196a-2 , TC