Circular RNAs (circRNAs), a special type of non-coding RNA molecules, have been addressed to be implicated in gastric cancer progression. The GSE93541 and GSE83521 microarrays found hsa-circRNA-000670 (hsa-circ-0000670) as an up-regulated circRNAin gastric cancer. We mainly investigated the function and molecular mechanisms of hsa-circ-0000670 involved in gastric cancer. The expression of hsa-circ-0000670 was determined by RT-qPCR to be highly expressed in gastric cancer tissues relative to corresponding adjacent normal tissues, as well as in gastric cancer cell lines relative to normal gastric mucosal epithelial cell line. By conducting EdU, scratch test and Transwell assays, hsa-circ-000670 was found to be a tumor promoter by potentiating the proliferative, invasive and migrating capabilities of gastric cancer cells. Consistently, a tumor-promotive role of hsa-circ-000670 was validated in vivo. Dual-luciferase reporter gene and RIP assays identified the binding of hsa-circ-0000670 to microRNA-384 (miR-384) and the binding of miR-384 to sine oculis-related homeobox 4 (SIX4). The oncogenic potential of hsa-circ-0000670 in gastric cancer cells were inhibited by overexpressed miR-384. Mechanistically, SIX4 was targeted by miR-384 and was upregulated in gastric cancer. High SIX4 expression was suggested to correlate with the poor prognosis of gastric cancer patients. Additionally, silencing of SIX4 delayed tumor growth and progression, which were reversed by overexpression of hsa-circ-0000670. Taken together, hsa-circ-0000670 acts as a tumor promotor in gastric cancer progression and might be a potential target for gastric cancer treatment.

环状RNA（circRNA）是一种特殊类型的非编码RNA分子，已被认为与胃癌的进展有关。GSE93541和GSE83521微阵列发现hsa-circRNA-000670（hsa-circ-0000670）作为胃癌中circRNA的上调。我们主要研究hsa-circ-0000670参与胃癌的功能和分子机制。通过RT-qPCR确定hsa-circ-0000670的表达在胃癌组织中相对于相应的相邻正常组织中高表达，并且在胃癌细胞系中相对于正常胃粘膜上皮细胞系高表达。通过进行EdU，划痕测试和Transwell分析，发现hsa-circ-000670通过增强胃癌细胞的增殖，侵袭和迁移能力而成为肿瘤启动子。一致地，体内。双荧光素酶报告基因和RIP分析鉴定了hsa-circ-0000670与microRNA-384（miR-384）的结合以及miR-384与正弦骨相关的同源盒4（SIX4）的结合。过度表达的miR-384抑制了hsa-circ-0000670在胃癌细胞中的致癌潜能。从机制上讲，SIX4被miR-384靶向并在胃癌中被上调。提示SIX4高表达与胃癌患者预后不良有关。此外，SIX4沉默可延缓肿瘤的生长和进展，而过度表达hsa-circ-0000670可以逆转肿瘤的生长和进展。综上所述，hsa-circ-0000670可作为胃癌进展中的肿瘤促进剂，并可能成为胃癌治疗的潜在靶标。