It is found that the inflammatory molecule interleukin-1 beta (IL1β) was reduced in PTC tissues and was associated with lymph node metastasis and was associated with lymph node metastasis.
Abstract
Simple Summary Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer (THCA), and although most patients have a good prognosis, some patients develop aggressive disease with lymph node metastasis and recurrence. Inflammation-related factors are increasingly recognized as important regulators of tumor development, but their roles in PTC remain unclear. In this study, we found that the inflammatory molecule interleukin-1 beta (IL1β) was reduced in PTC tissues and was associated with lymph node metastasis. Increasing IL1β levels inhibited tumor cell growth, migration, invasion, and promoted cancer cell death. Further investigation revealed that IL1β suppressed tumor progression by increasing SMDT1 gene expression and reducing MAPK signaling activity. These findings provide new insights into how inflammatory signals regulate THCA progression and suggest potential biomarkers and therapeutic targets for patients with aggressive PTC.
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