Downregulation of miR-146b-5p via iodine involvement repressed papillary thyroid carcinoma cell proliferation

Author:

Pan Yujia123,Yun Weikang4,Shi Bingshuai5,Cui Rongjun2,Liu Chi2,Ding Zhong6,Fan Jialin2,Jiang Wenqian2,Tang Jiebing7,Zheng Tianhu2,Yu Xiaoguang2,Liu Ying1

Affiliation:

1. 1Key Lab of Etiology and Epidemiology, National Health and Family Planning Commission, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, Heilongjiang, China

2. 2Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, China

3. 3College of Medical Laboratory Science, Guilin Medical University, Guilin, Guangxi, China

4. 4Department of Radiation Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China

5. 5Department of Thyroid Surgery, First Affiliated Hospital of Henan University, Kaifeng, Henan, China

6. 6Kaifeng Center for Disease Prevention and Control, Kaifeng, Henan, China

7. 7Department of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China

Abstract

miR-146b-5p is overexpressed in papillary thyroid carcinoma (PTC) and is thought to be a related diagnostic marker. Previous studies have indicated the effects of iodine on oncogenic activation. However, the effect of iodine on the proliferation of PTC cells and the associated underlying mechanisms remain unclear. We found that miR-146b-5p was downregulated and smad4 was upregulated in patients exposed to high iodine concentration by in situ hybridisation (ISH) and immunohistochemical (IHC). NaI (10−3 M) treatment downregulated miR-146b-5p and upregulated Smad4 in PTC cell lines. Luciferase assay was used to confirm that Smad4 is a target of miR-146b-5p. Furthermore, MTT assay and cell cycle analysis indicated that 10−3 M NaI suppressed cell proliferation and caused G0/G1 phase arrest. Real-time PCR and Western blotting demonstrated that 10−3 M NaI increased p21, p27, and p57 levels and reduced cyclin D1 levels in PTC cells. Our findings suggest that 10−3 M NaI increases Smad4 levels through repression of miR-146b-5p expression, curbing the proliferation in PTC.

Publisher

Bioscientifica

Subject

Endocrinology,Molecular Biology

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