Physical Examination Center, Cangzhou Central Hospital, Cangzhou, Hebei, China.
Department of Gastroenterology, Cangzhou Central Hospital, Cangzhou, Hebei, China.
Cell Biochem Funct. 2020 Dec;38(8):1017-1024. doi: 10.1002/cbf.3532. Epub 2020 Jun 3.
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. SIGNIFICANCE OF THE STUDY: Papillary thyroid cancer (PTC) is the most important pathological type of thyroid cancer, accounting for 80% of thyroid cancer. miR-124-3p exhibited significant inhibitory role in the transformation and development of malignant tumours. However, in PTC, the roles and its potential molecular mechanism are unclear. Here, the study investigated the roles of miR-124-3p in the progress of PTC and its potential molecular mechanism. We found that miR-124-3p inhibited the proliferation and motility, and induced apoptosis and cell cycle arrest in PTC cells. This study provided a novel molecular mechanism of miR-124-3p in the progress of PTC.
本研究旨在探讨 miR-124-3p 及其潜在分子机制在甲状腺乳头状癌(PTC)中的作用。通过 RT-qPCR 检测人甲状腺滤泡上皮细胞系(NTHY-ORI3-1)和人甲状腺乳头状癌细胞系(SW1736、BCPAP、TPC-1 和 K1)中 miR-124-3p 和丝裂原活化蛋白激酶 4(MAP2K4)的表达。通过 CCK-8 检测细胞增殖,通过流式细胞术检测细胞周期和凋亡率。通过 Transwell 测定和划痕愈合测定分别测定侵袭能力和迁移能力。Western blot 用于检测相对蛋白水平。在体内,将转染 miR-124-3p 模拟物的 TPC-1 细胞皮下注射到小鼠的侧腹形成肿瘤。建模成功后,将小鼠分为两组(n=10):对照组和 miR-124-3p 模拟物组。本研究表明,miR-124-3p 在 PTC 细胞系中低表达,而 MAP2K4 高表达。此外,miR-124-3p 在 TPC-1 细胞中靶向 MAP2K4 并负调控 MAP2K4。此外,miR-124-3p 通过激活 MAP2K4/JNK/JunD 通路抑制 TPC-1 细胞的增殖和迁移,诱导细胞凋亡和细胞周期停滞。此外,miR-124-3p 通过下调体内 MAP2K4 水平抑制肿瘤形成。综上所述,本研究为 miR-124-3p 在 PTC 进展中的作用提供了一个新的分子机制。
甲状腺乳头状癌(PTC)是甲状腺癌最重要的病理类型,占甲状腺癌的 80%。miR-124-3p 在恶性肿瘤的转化和发展中具有显著的抑制作用。然而,在 PTC 中,其作用及其潜在的分子机制尚不清楚。在这里,我们研究了 miR-124-3p 在 PTC 进展中的作用及其潜在的分子机制。我们发现 miR-124-3p 抑制 PTC 细胞的增殖和迁移,并诱导细胞凋亡和细胞周期停滞。本研究为 miR-124-3p 在 PTC 进展中的作用提供了一个新的分子机制。