LINC01116 promotes the progression of papillary thyroid carcinoma by regulating the apoptosis of bone marrow mesenchymal stem cells

Abstract: Background: Papillary thyroid carcinoma (PTC) is a common endocrine malignancy with rising incidence. The role of LINC01116 in PTC progression and its underlying mechanisms remain unclear. Objectives: To investigate LINC01116 expression in PTC, evaluate its prognostic significance and explore its functional role in regulating bone marrow mesenchymal stem cell (BMSC) apoptosis. Methods: This was a cross-sectional observational study with a prognostic cohort component.Serum samples from 60 PTC patients and 30 healthy controls were analyzed by RT-qPCR. Prognostic value was assessed using Kaplan-Meier survival analysis and Cox regression. In vitro, LINC01116 expression was manipulated in PTC cells and BMSCs using three independent siRNAs and pcDNA3.1 overexpression plasmids. Cell proliferation was evaluated by CCK-8 and colony formation assays, migration by Transwell assays and apoptosis by flow cytometry and Western blot analysis of Bcl-2, cleaved caspase-3 and cleaved caspase-9. Rescue experiments using siRNA-resistant LINC01116 were performed to confirm specificity. Results: LINC01116 was significantly upregulated in serum from PTC patients compared with healthy controls (P < 0.001). High LINC01116 expression correlated with advanced TNM stage and predicted reduced disease-free survival (HR=2.067, P=0.026) and overall survival (HR=2.081, P=0.024), serving as an independent prognostic factor. Knockdown of LINC01116 inhibited PTC cell proliferation and migration, while overexpression enhanced these effects. Mechanistically, LINC01116 suppressed BMSC apoptosis by upregulating Bcl-2 and downregulating cleaved caspase-3/9. Knockdown of LINC01116 induced opposite effects. Rescue experiments confirmed that restoring LINC01116 expression partially reversed knockdown-induced phenotypes (50-60% reversal), demonstrating functional specificity. Conclusion: LINC01116 is significantly upregulated in PTC and serves as an independent prognostic biomarker. It promotes tumor progression by inhibiting BMSC apoptosis through modulation of the Bcl-2/caspase pathway. These findings provide new insights into PTC pathogenesis and suggest LINC01116 as a potential therapeutic target.