Autophagy in cancer associated fibroblasts promotes lung adenocarcinoma cells migration and invasion

Objective Autophagy is a process by which cellular material is delivered to lysosomes for degradation, providing energy and macromolecular precursors. Cancer-associated fibroblasts (CAFs) have an important role in reprogramming the tumor microenvironment, and exhibit enhanced migratory capacity through autocrine and paracrine. This study aims to explore the possible effects of CAFs autophagy on lung adenocarcinoma cells migration and invasion. Methods Lung adenocarcinoma cell line A549 was co-cultured with or without CAFs via Transwell and Matrige lassay under the same culture condition, the effects of CAFs autophagy on the migration and invasion of A549 were observed. Results We demonstrate autophagy activated CAFs have great ability than CAFs to enhance the migration [(122.7±17.6) cells/cm2 vs. (269.3±72.7) cells/cm2] and invasion [(124.3±19.6) cells/cm2 vs. (280.0±32.1) cells/cm2] of lung adenocarcinoma (LUAD) cell line (F=18.640, 80.630, P<0.05). Interleukin 6 [(545.5±28.2) ng/L vs. (865.4±70.9) ng/L] and interleukin 8 [(374.2±62.2) ng/L vs. (672.4±24.2) ng/L] were highly expressed in the autophagy activated CAFs conditioned media (t=7.261, 7.738, P<0.05). Conclusion Our results establish an oncogenic function for secretory autophagy in CAFs that promote LUAD migration and invasion. Key words: Lung adenocarcinoma; Cancer-associated fibroblasts; Autophagy; Migration and invasion