Study on the mechanism of interleukine-11 promoting anaplastic thyroid carcinoma cells invasion and metastasis

Objective To explore the mechanism of hypoxia inducing interleukine (IL)-11 secretion in anaplastic thyroid carcinoma (ATC) cells and the mechanism of IL-11 promoting epithelial mesenchymal transition of ATC cells. Methods Knockdown of IL-11, hypoxia-inducible factor (HIF)-1α in ATC cells or treatment of ATC cells with Cobalt Chloride, recombinant human interleukin (rhIL)-11, IL-11 antibody, then the effects of these interventions on the invasion and migration ability of ATC cells and its mechanism were detected by enzyme-linked immunosorbent assay (ELISA), Transwell, Real-time polymerase chain reaction (PCR), Western blotting. Results Under treatment with Cobalt Chloride, the protein and mRNA expression of IL-11 increased in ATC cells. The number of invasive cells in the knockdown HIF-1α group (61.7±4.9, 30.0±4.6) was less than that of the control group 261.7±8.7 (P<0.01), and the number of migrated cells (87.3±4.5, 73.8±5.4) was less than the control group 337.3±7.1 (P<0.01). The expression ofphosphorylated Akt (p-Akt), phosphorylated glycogen synthase kinase 3β (p-GSK3β) and Snail protein was significantly increased after treatment with rhIL-11. The protein expression of p-Akt, p-GSK3β and Snail were significantly decreased after knockdown of IL-11 expression in ATC cells. Conclusion Hypoxia induced epithelial mesenchymal transition of ATC cells is the main mechanism of high invasion and migration of ATC cells. Key words: Anaplastic thyroid carcinoma; Interleukine-11; Epithelialmesenchymal transition; Invasion and metastasis