Circ-sirt1 inhibits growth and invasion of gastric cancer by sponging miR-132-3p/miR-212-3p and upregulating sirt1 expression
| Autor: | Yuan-Ting Liu, Bing-Hui Li, Jing-Wu Li, Yankun Liu, Qing-Ke Li, Yufeng Li |
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| Rok vydání: | 2021 |
| Předmět: |
Cancer Research
animal structures endocrine system diseases Cell Mice miR-132 Sirtuin 1 Stomach Neoplasms Cell Line Tumor medicine Animals Humans Tumor growth Tumor xenograft Cell Proliferation Gene knockdown Chemistry Cancer medicine.disease MicroRNAs enzymes and coenzymes (carbohydrates) Real-time polymerase chain reaction medicine.anatomical_structure Oncology Cancer research MiR-212 biological phenomena cell phenomena and immunity hormones hormone substitutes and hormone antagonists |
| Zdroj: | Neoplasma. 68:780-787 |
| ISSN: | 1338-4317 |
| DOI: | 10.4149/neo_2021_210218n222 |
| Popis: | circRNAs have been considered as a rising factor in cancers. However, the roles and mechanisms of circ-sirt1 in gastric cancer (GC) remain largely unknown. In this study, we found that the expressions of sirt1 and circ-sirt1 are decreased in tissues or serums of GC patients by real-time quantitative PCR (RT-qPCR). The expressions of miR-132-3p/miR-212-3p showed an opposite tendency in these samples. The co-transfection of miR-132-3p/miR-212-3p mimics counteracted the enhancement of sirt1 expression induced by circ-sirt1. The results of cell colony-formation assay and transwell assays demonstrated that the proliferation, migration, and invasion activities of BGC-823 cells were inhibited by circ-sirt1 overexpression or miR-132-3p/miR-212-3p knockdown, respectively. The xenograft tumor model result indicated that the circ-sirt1 overexpression suppressed the tumor growth of BGC-823 cells. The regulation of miR-132-3p/miR-212-3p between circ-sirt1 and sirt1 was verified in the mice tumor tissues. Thus, circ-sirt1 inhibited tumor growth and invasion probably by sponging miR-132-3p/miR-212-3p and upregulating sirt1 expression in GC. These findings may provide a theoretical basis for the classification of GC and a novel therapeutic target for GC patients. |
| Databáze: | OpenAIRE |
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