Although papillary thyroid cancer (PTC) has a generally decent prognosis, approximately 10% of patients experience recurrence, which is frequently associated with distant metastasis. Stomatin-like protein 2 (SLP-2), a protein located in the mitochondrial intermembrane space, is thought to be a possible cancer promoter. This study aimed to discover the involvement of SLP-2 in PTC motility and angiogenesis, and to initially explore its mechanism. According to the CCLE database, SLP-2 was universally increased in various cancers. Then SLP-2 expression in PTC cell lines was evaluated. Thereafter the influences of SLP-2 knockdown on cell migration, invasion, epithelial-mesenchymal transition (EMT), and angiogenesis were assessed, respectively. The mediated roles of reactive oxygen species (ROS) and MAPKs in the SLP-2 regulation were likewise determined. SLP-2 was discovered to be upregulated in PTC cells, and its knockdown could suppress cell migration, invasion, EMT, and angiogenesis. Declined SLP-2 expression also facilitated ROS generation and inhibited phosphorylation of MAPKs. Moreover, ERK agonist and ROS scavenger treatment partially reversed the impacts of SLP-2 knockdown on cells, indicating SLP-2 regulated generation of ROS and ERK pathway to promote PTC motility and angiogenesis. Generally, SLP-2 appears to be one of the major genes in the pathogenesis of PTC. Silencing its expression may have an impact on the onset and evolution of PTC. The fact that SLP-2 has a considerable influence on ROS levels implies that PTC can be treated by boosting ROS levels.
Keywords: Angiogenesis; MAPK; Papillary thyroid cancer; Reactive oxygen species; Stomatin-like protein 2.
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