Thyroid cancer is a common malignant tumour of the endocrine system and ranks ninth in cancer incidence worldwide. An extensive body of evidence has demonstrated that lncRNAs play a critical role in the progression of thyroid cancer. The lncRNA MAPKAPK5-AS1 has been reported to be abnormally expressed and to play a role in the development of various human cancers. However, MAPKAPK5-AS1’s potential role in thyroid cancer progression remains unknown. The objective of our study was to explore the role and mechanism of MAPKAPK5-AS1 in thyroid cancer cells and provide a potential target for its biological diagnosis and treatment. We transfected sh-MAPKAPK5-AS1 and sh-NC into BCPAP and TPC-1 cells for loss-of-function assays. Results of RT-qPCR analysis demonstrated that MAPKAPK5-AS1 was more highly expressed in thyroid cancer cells compared to normal cells. Functional assays demonstrated that interfering with the expression of MAPKAPK5-AS1 notably repressed proliferation and invasion and accelerated apoptosis of BCPAP and TPC-1 cells. Mechanistically, we found that miR-519e-5p was negatively regulated by MAPKAPK5-AS1 and that tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein eta (YWHAH) was a target of miR-519e-5p. Additionally, rescue assays demonstrated that downregulation of MAPKAPK5-AS1 expression inhibited cell proliferation, migration, and invasion and promoted apoptosis by sponging miR-519e-5p, thereby increasing YWHAH expression. Ultimately, our study revealed that MAPKAPK5-AS1 promotes proliferation and migration of thyroid cancer cells by targeting the miR-519e-5p/YWHAH axis, which provides novel insight into the development and progression of thyroid cancer.

甲状腺癌是内分泌系统的常见恶性肿瘤，在全球癌症发病率中排名第九。大量证据表明，lncRNA在甲状腺癌的进展中起关键作用。据报道，lncRNA MAPKAPK5-AS1异常表达并在各种人类癌症的发展中发挥作用。然而，MAPKAPK5-AS1在甲状腺癌进展中的潜在作用仍然未知。我们的研究目的是探讨MAPKAPK5-AS1在甲状腺癌细胞中的作用和机制，为其生物学诊断和治疗提供潜在的靶标。我们将sh-MAPKAPK5-AS1和sh-NC转染到BCPAP和TPC-1细胞中，以进行功能丧失检测。RT-qPCR分析的结果表明，与正常细胞相比，MAPKAPK5-AS1在甲状腺癌细胞中的表达更高。功能测定表明，干扰MAPKAPK5-AS1的表达显着抑制了BCPAP和TPC-1细胞的增殖和侵袭并加速了细胞凋亡。从机理上讲，我们发现miR-519e-5p受MAPKAPK5-AS1负调控，酪氨酸3-单加氧酶/色氨酸5-单加氧酶激活蛋白eta（YWHAH）是miR-519e-5p的目标。此外，救援分析表明，通过使miR-519e-5p变海绵，MAPKAPK5-AS1表达的下调抑制了细胞的增殖，迁移和侵袭，并促进了细胞凋亡，从而增加了YWHAH的表达。最终，