Papillary thyroid carcinoma (PTC) is a prevalent endocrine malignancy with a high incidence rate of regional lymph node metastasis. Dysregulation of lncRNA XIST has been observed in various malignancies. This study aims to elucidate the molecular mechanism of lncRNA XIST in PTC metastasis. Quantitative real-time PCR assays were conducted to detect the expression levels of XIST, FN1, and miR-204-5p in PTC tissues. Meanwhile, loss-of-function assays were employed to evaluate the oncogenic roles of XIST in PTC cell lines. Our results revealed significant overexpression of XIST and FN1 in PTC tissues and cell lines, accompanied by decreased levels of miR-204-5p ( < 0.05). Knockdown of XIST or FN1 inhibited cellular proliferation, metastasis, and invasion in PTC cells, upregulated E-cadherin, and downregulated N-cadherin and Vimentin. Furthermore, we demonstrated that XIST regulates FN1 expression by competitively binding to miR-204-5p. MiRNA inhibitor rescue assays confirmed the pivotal role of the XIST/miR-204/FN1 axis in PTC metastasis and invasion. Our study underscores the oncogenic role of XIST in PTC by acting as a sponge for miR-204, regulating FN1 expression. These findings hold promise for advancing our understanding of thyroid cancer and developing potential therapeutic and diagnostic targets for PTC.