The study aimed to investigate the role of miR‐124‐3p and its potential molecular mechanism in papillary thyroid cancer (PTC). The expression of miR‐124‐3p and mitogen‐activated protein kinase 4 (MAP2K4) in human thyroid follicular epithelial cell line (NTHY‐ORI3‐1) and human papillary thyroid carcinoma cell lines (SW1736, BCPAP, TPC‐1 and K1) was measured by RT‐qPCR. Cell proliferation was measured by CCK‐8, while cell cycle and apoptosis rate were measured by flow cytometry. Invasive ability and migrative ability were measured by transwell assay and wound healing assay, respectively. Western blot was used to detect the levels of relative proteins. In vivo, TPC‐1 cells transfected with miR‐124‐3p mimic were subcutaneously injected into the flank of the mice to form tumour. After successful modelling, mice were divided into two groups (n = 10): Control group and miR‐124‐3p mimic group. The present study showed that miR‐124‐3p was lowly expressed, while MAP2K4 was highly expressed in PTC cell lines. Besides, miR‐124‐3p targeted MAP2K4 and negatively regulated MAP2K4 in TPC‐1 cells. In addition, miR‐124‐3p inhibited the proliferation and motility, and induced apoptosis and cell cycle arrest of TPC‐1 cells by inactivating MAP2K4/JNK/JunD pathway. Furthermore, miR‐124‐3p inhibited tumour formation by downregulating MAP2K4 level in vivo. In conclusion, the study provided a novel molecular mechanism of miR‐124‐3p in the progress of PTC.

中文翻译：

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microRNA-124-3p通过靶向甲状腺乳头状癌中的促分裂原活化蛋白激酶4抑制肿瘤发生。

该研究旨在研究miR‐124‐3p在甲状腺乳头状癌（PTC）中的作用及其潜在的分子机制。miR-124-3p和促分裂原活化蛋白激酶4（MAP2K4）在人甲状腺滤泡上皮细胞系（NTHY-ORI3-1）和人乳头状甲状腺癌细胞系（SW1736，BCPAP，TPC-1和K1）中的表达通过RT-qPCR测定。用CCK-8测定细胞增殖，用流式细胞术测定细胞周期和凋亡率。通过transwell测定法和伤口愈合测定法分别测定侵袭能力和迁移能力。使用蛋白质印迹法检测相对蛋白的水平。在体内，将经miR-124-3p模拟物转染的TPC-1细胞皮下注射到小鼠的腹侧面形成肿瘤。成功建模后，将小鼠分为两组（n = 10）：对照组和miR‐124‐3p模拟组。本研究表明，在PTC细胞系中miR-124-3p的表达较低，而MAP2K4的表达较高。此外，miR‐124‐3p靶向TPC‐1细胞中的MAP2K4和负调控的MAP2K4。此外，miR-124-3p通过失活MAP2K4 / JNK / JunD途径抑制TPC-1细胞的增殖和运动，并诱导其凋亡和细胞周期停滞。此外，miR-124-3p通过在体内下调MAP2K4水平来抑制肿瘤形成。总之，这项研究为PTC的发展提供了一种新的miR-124-3p分子机制。miR-124-3p通过失活MAP2K4 / JNK / JunD途径抑制TPC-1细胞的增殖和运动，并诱导其凋亡和细胞周期停滞。此外，miR-124-3p通过在体内下调MAP2K4水平来抑制肿瘤形成。总之，这项研究为PTC的发展提供了一种新的miR-124-3p分子机制。miR-124-3p通过失活MAP2K4 / JNK / JunD途径抑制TPC-1细胞的增殖和运动，并诱导其凋亡和细胞周期停滞。此外，miR-124-3p通过在体内下调MAP2K4水平来抑制肿瘤形成。总之，这项研究为PTC的发展提供了一种新的miR-124-3p分子机制。