Hsa_circ_0017728 as an oncogene in gastric cancer by sponging miR-149 and modulating the IL-6/STAT3 pathway

Hsa_circ_0017728 通过吸收 miR-149 并调节 IL-6/STAT3 通路,成为胃癌中的致癌基因

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作者:Chun Yang, Shaoping Deng

Conclusions

The regulatory network of hsa_circ_0017728/miR-149/IL-6/STAT3 cascade signaling might provide a better understanding of gastric carcinogenesis and progression.

Material and methods

High-throughput sequencing was used to determine differentially expressed circRNAs in GC tissues and corresponding non-cancerous tissues. The CCK-8 assay and Annexin V-fluorescein isothiocyanate/polyimide (Annexin V-FITC/PI) staining were performed to detect the cell viability and apoptosis in GC cells. In addition, gene expression and protein levels in GC tissues and cell lines were measured using RT-qPCR and western blotting, respectively.

Methods

High-throughput sequencing was used to determine differentially expressed circRNAs in GC tissues and corresponding non-cancerous tissues. The CCK-8 assay and Annexin V-fluorescein isothiocyanate/polyimide (Annexin V-FITC/PI) staining were performed to detect the cell viability and apoptosis in GC cells. In addition, gene expression and protein levels in GC tissues and cell lines were measured using RT-qPCR and western blotting, respectively.

Results

Our results demonstrated that the hsa_circ_0017728 expression level was up-regulated in GC tissues and cell lines and closely associated with poor overall survival and pathological differentiation, higher TNM stage and lymph node metastasis. Knockdown of hsa_circ_0017728 had the ability to cause inhibition of cell proliferation and migration and elevate the cell apoptosis rate in GC cells. We also discovered that hsa_circ_0017728 might serve as a ceRNA to sponge miR-149 and indirectly regulated the IL-6/STAT3 signaling pathway in GC cell proliferation and apoptosis. Conclusions: The regulatory network of hsa_circ_0017728/miR-149/IL-6/STAT3 cascade signaling might provide a better understanding of gastric carcinogenesis and progression.

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