Sciellin promotes the development and progression of thyroid cancer through the JAK2/STAT3 signaling pathway.

ABSTRACT

Thyroid cancer (TC) is one of the most common endocrine tumors worldwide. Sciellin (SCEL) is involved in various disease processes, including burn wound healing and neutrophil extracellular traps (NETs); it is highly expressed in TC. However, its biological impact on TC and related mechanisms remain unclear. This study aimed to investigate the effect of SCEL on the function of human TC cell lines B-CPAP and OCUT-2C (cancer cell lines with BRAF V600E mutations). Analyses of data sets and clinical samples revealed enhanced expression of SCEL in TC than in adjacent normal tissue. SCEL knockout suppresses proliferation and cell cycle progression in TC cells, and these results were reversed by the upregulated SCEL expression in TC. SCEL knockout inhibited tumor development in xenograft mouse models. Western blot (WB) demonstrated that the expression of p-JAK2 and p-STAT3 was reduced in SCEL-knockdown TC. These results suggest that SCEL plays a key role in TC progression through the JAK2-STAT3 pathway. Therefore, SCEL can be considered a potential diagnostic biomarker and therapeutic target for TC.