Recombinant Human IL-11 Promotes Lung Adenocarcinoma A549 Cell Growth and EMT through Activating STAT3/HIF-1α/EMT Signaling Pathway.

BACKGROUND Interleukin-11 (IL-11) could promote invasion and metastasis of cancer cells, however, its mechanism is unclear. OBJECTIVE This study aimed to investigate effects of recombinant human IL-11 (rhIL-11) on lung cancer cell metastasis and growth. METHODS Human lung cancer cell, A549, was cultured and subcutaneously injected into mice to establish Xenograft tumor models. Tumor models were divided into Control, rhIL-11 transplantation (250 μg/kg/day), rhIL-11 transplantation (500 μg/kg/day) group. Tumor volumes were recorded and measured for 6 times. Hypoxia inducible factor 1α (HIF1α), Snail, Slug, signal transducers/activators of transcription-3 (STAT3), E-cadherin, Twist, Vimentin levels were evaluated using western blot and real-time PCR (RT-PCR). RESULTS Sizes of subcutaneous tumors were increased following with measurement time. rhIL-11 treatment significantly enhanced HIF1α and STAT3 expression in rhIL-11 treatment groups compared to Control group (p 0.05). rhIL-11 treatments significantly increased Twist, Slug expressions compared to Control group (p<0.05). Especially for rhIL-11 (500 μg/kg/day) treatment, which triggered significantly higher effects on Twist and Slug expressions compared to those in Control group (p<0.05). Vimentin and Snail mRNA levels were significantly up-regulated and E-cadherin level was significantly down-regulated in rhIL-11 treatment groups compared to Control group (p<0.05). Meanwhile, rhIL-11 at dosage of 500 μg/kg/day triggered remarkably higher effects on Vimentin, Snail, Ecadherin expressions compared to those in rhIL-11 (250 μg/kg/day) group (p<0.05). CONCLUSION rhIL-11 transplantation promoted growth and epithelial-mesenchymal transition (EMT) of A549 cells, which might be associated to STAT3/HIF-1α/EMT signaling pathway activation.