Long non-coding RNA FAM83H-AS1 induced by adipose-derived stem cells promotes breast and pancreatic cancer cell proliferation and migration

Background: Stromal cells recruited to the tumor microenvironment and long non-coding RNAs (lncRNAs) in the tumor cells regulate cancer progression. However, their relationship is largely unknown. Methods In the current study, we identified the effects of lncRNA FAM83H-AS1, induced by adipose-derived stem cells (ADSCs) during tumor development, and explored the underlying mechanisms using a coculture cell model. Adipose tissues were obtained from healthy female donors, the expression of stromal markers on cell surface of expanded ADSCs were confirmed using immunofluorescence analysis. The breast and pancreatic cancer cells were cultured with or without ADSCs using 24-well transwell chamber systems with 8.0 µm pore size. Results Our results showed that FAM83H-AS1 was upregulated in breast and pancreatic cancers and associated with poor prognosis. ADSCs further induced FAM83H-AS1 and increased tumor cell proliferation via promoting G1/S transition through cyclin D1, CDK4 and CDK6. Wound healing, modified Boyden chamber and immunoblotting assays demonstrated that ADSCs induced epithelial-mesenchymal transition and migration of breast and pancreatic cancer cells in a FAM83H-AS1-dependent manner. And ADSC-induced FAM83H-AS1 increased unfolded protein response through AKT/XBP1 pathway. Conclusion In conclusion, our results indicated that ADSCs promoted breast and pancreatic cancer development via inducing cell proliferation and migration, as well as unfolded protein response through FAM83H-AS1.