Background
Gastric cancer (GC) is a common and deadly malignancy in the world. CircRNAs have emerged as important regulators in human diseases, including GC. In this work, we intended to explore the role of circ_CORO1C in GC progression and potential mechanism.
Conclusion
Depletion of circ_CORO1C suppressed GC progression by regulating miR-138-5p/KLF12 axis, offering a potential molecular target for GC therapy.
Methods
Quantitative real-time PCR (qRT-PCR) or Western blot assay was performed to examine the expression of circRNA coronin-like actin-binding protein 1C (circ_CORO1C), microRNA (miR)-138-5p and Krueppel-like factor 12 (KLF12) in clinical samples and cells. Cell colony formation ability and viability were measured by colony formation assay and methyl thiazolyl tetrazolium (MTT) assay, respectively. Expression of cell proliferation and epithelia-mesenchymal transition (EMT) biomarker was detected by Western blot analysis. And cell metastasis, including migration and invasion, and apoptosis were analyzed via Transwell assay and flow cytometry, respectively. Target relationship among circ_CORO1C, miR-138-5p and KLF12 was validated by dual-luciferase reporter assay. The in vivo role of circ_CORO1C was investigated by tumor xenograft assay.
Results
Circ_CORO1C and KLF12 were upregulated, while miR-138-5p was downregulated in GC tissues and cells. Circ_CORO1C knockdown suppressed colony formation ability, viability, migration, invasion and EMT in GC cells, while promoted cell apoptosis in vitro. Circ_CORO1C targeted miR-138-5p, the inhibition of which could attenuate silenced circ_CORO1C-induced inhibitory effects on GC progression. MiR-138-5p repressed the aggressive malignant behaviors of GC cells by directly targeting KLF12. Circ_CORO1C deficiency inhibited GC tumor growth in vivo.