G protein subunit alpha 15 (GNA15) is recognized as an oncogene for some cancers, however, its role in thyroid carcinoma (TC) is elusive and is investigated in this study. Concretely, bioinformatics was employed to analyze the GNA15 expression profile in TC. The effect of GNA15 on TC cell functions was examined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, and Transwell assays. Expressions of extracellular regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 were determined using Western blot. The involvement of Bruton tyrosine kinase (BTK) in the mechanism of GNA15 was investigated by BTK knockdown and rescue assay. GNA15 presented an overexpression pattern in TC samples, which facilitated the viability, proliferation, migration, and invasion of TC cells; GNA15 silencing led to converse results. Ratios of p-ERK/ERK, p-JNK/JNK, and p-p38/p38 were upregulated by GNA15 overexpression. The BTK deficiency weakened the aforementioned behaviors of TC cells and blocked the MAPK signaling pathway, however, these effects were counteracted by GNA15 overexpression. Collectively, GNA15 contributes to the malignant development of TC cells by binding to BTK and thus activating the MAPK signaling pathway.

中文翻译：

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GNA15通过BTK介导的MAPK信号通路促进甲状腺癌细胞的恶性发展。

G 蛋白亚基 α 15 (GNA15) 被认为是某些癌症的癌基因，但其在甲状腺癌 (TC) 中的作用尚不清楚，本研究对其进行了研究。具体而言，采用生物信息学分析TC中GNA15的表达谱。使用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑 (MTT)、集落形成和 Transwell 测定检查 GNA15 对 TC 细胞功能的影响。使用蛋白质印迹法测定细胞外调节蛋白激酶 (ERK)、c-Jun N 末端激酶 (JNK) 和 p38 的表达。通过 BTK 敲除和救援实验研究了 Bruton 酪氨酸激酶 (BTK) 在 GNA15 机制中的参与。 GNA15在TC样本中呈现过度表达模式，促进TC细胞的活力、增殖、迁移和侵袭； GNA15 沉默导致相反的结果。 GNA15 过表达会上调 p-ERK/ERK、p-JNK/JNK 和 p-p38/p38 的比率。 BTK缺陷削弱了TC细胞的上述行为并阻断了MAPK信号通路，然而，这些影响被GNA15过表达所抵消。总的来说，GNA15通过与BTK结合从而激活MAPK信号通路而促进TC细胞的恶性发展。