Objective To investigate the expression characteristics of TGFB1–TGF-β/Smad signaling in papillary thyroid carcinoma (PTC) and its association with invasion-related phenotypes. Methods Tumor tissues and paired adjacent normal tissues were collected from 31 patients with PTC. TGFB1 mRNA expression was detected using quantitative real-time PCR (qPCR), and TGFβ-1 protein expression was evaluated by Western blot. Immunohistochemistry combined with QuPath software was used to quantify the tissue localization and expression intensity of TGFβ-1 and its downstream molecule p-Smad2/3. Samples were stratified according to extrathyroidal extension (ETE) and lymph node metastasis (LNM), and comparisons were performed both within and between stratified groups based on paired tumor–normal tissues. Results TGFB1 mRNA expression was significantly higher in tumor tissues than in paired adjacent tissues (P < 0.05), and this difference was consistently observed within ETE and LNM subgroups, whereas no significant differences were found between stratified groups. Western blot analysis showed no significant difference in overall TGFβ-1 protein expression. Immunohistochemistry revealed that TGFβ-1 was mainly localized in the cytoplasm of tumor cells and was significantly elevated in tumor tissues compared with adjacent tissues. p-Smad2/3 exhibited marked nuclear localization in tumor tissues, indicating activation of the TGF-β/Smad pathway. Stratified analysis showed that nuclear localization of p-Smad2/3 was relatively more pronounced in the No-ETE and N0 subgroups, whereas this difference tended to weaken in ETE and N1 samples. Conclusion TGFB1 transcription is upregulated in PTC, and TGF-β1 expression is increased in tumor tissues. Differential nuclear localization of p-Smad2/3 across invasion-related stratifications suggests a potential stage-dependent regulatory role of the TGF-β/Smad pathway in PTC invasion.