LncRNA CARLo-7 facilitates proliferation, migration, invasion, and EMT of bladder cancer cells by regulating Wnt/β-catenin and JAK2/STAT3 signaling pathways.

Abstract

BackgroundAberrant expression of long noncoding RNAs (lncRNAs) has been found to enroll in the initiation and progression of bladder cancer (BC). Earlier results show cancer-associated region long noncoding RNA-7 (CARLo-7) can be a prognostic marker for BC, but its biological function and the underlying mechanism is still to be discovered. Our study aims to explore the effects of CARLo-7 on the initiation and progression of BC and the potential mechanisms.MethodsThe expression of CARLo-7 in BC tissues and cell lines was determined by quantitative real-time polymerase chain reaction (qRT-PCR). T24 and HT1197 cells were transfected with CARLo-7 expression vector or sh-CARLo-7, then cell viability assay, BrdU assay, flow cytometry, Transwell cell migration, and invasion assay, and western blot were conducted to evaluate cell proliferation, apoptosis, invasion, migration, and epithelial-mesenchymal transition (EMT).ResultsCARLo-7 was dramatically upregulated in BC tissues and cell lines. Silencing CARLo-7 by sh-CARLo-7 significantly suppressed proliferation and induced apoptosis of BC cells, while enforced CARLo-7 expression promoted cell proliferation. Meanwhile, silencing CARLo-7 attenuated migration, invasion, and EMT of BC cells, while CARLo-7 overexpression had the contrary effects. The β-catenin, p-JAK2 and p-STAT3 levels were decreased by CARLo-7 knockdown, while activation of Wnt/β-catenin or JAK2/STAT3 pathways abolished the effects of CARLo-7 knockdown on cell proliferation and migration.ConclusionsCollectively, CARLo-7 plays a critical role in regulating BC development by regulating cell proliferation, migration, invasion, and EMT through Wnt/β-catenin and JAK2/STAT3 signaling. Therefore, CARLo-7 might be a promising therapeutic target for BC.