非小细胞肺癌 (non-small cell lung cancer, NSCLC) 是世界上最常见和致命的癌症之一。循环RNA (circular RNA, circRNA) 可广泛参与 NSCLC 的发生和发展过程。然而，circRNA 在 NSCLC 中的调控机制仍然不明确。本研究旨在探究 circ_0101675 在 NSCLC 进展中的潜在作用。我们通过定量实时聚合酶链反应检测了 NSCLC 组织和细胞中 circ_0101675、microRNA-607(miR-607) 和程序性细胞死亡受体配体1(programmed cell death receptor ligand 1, PDL1) 的表达。我们利用细胞计数试剂盒 8、集落形成实验、划伤愈合实验、Transwell 实验、管状形成实验和流式细胞术对 NSCLC 细胞的增殖、迁移、侵袭、血管生成和凋亡进行了检测。我们将 NSCLC 细胞与外周血单个核细胞共培养来评估免疫反应。我们通过免疫印迹测定测定 PDL1 和与凋亡相关的蛋白的水平。我们进行了双荧光素酶报告基因试验和 RNA 免疫沉淀实验，以验证 miR-607 与 circ_0101675 或 PDL1 之间的直接靶位点。我们采用体内实验探究 circ_0101675 对 NSCLC 肿瘤生长的影响。NSCLC 细胞和癌组织中 circ_0101675 和 PDL1 的表达高，而 miR-607 的表达低。抑制 circ_0101675 能够抑制 NSCLC 细胞的生长、迁移、侵袭、血管生成和免疫逃逸。从机制上讲，我们发现 circ_0101675 的高水平可以通过吸附 miR-607 来上调 PDL1 的表达。此外，减少 circ_0101675 能够通过增强 miR-607 的表达来降低 PDL1 的表达，从而抑制 NSCLC 肿瘤在体内的生长。总之，我们的结果表明，circ_0101675 可能通过 miR-607/PDL1 轴促进 NSCLC 的增殖、迁移、侵袭和免疫逃避能力。© 2023 该作者，Springer Science+Business Media, LLC, Springer Nature 的独家许可。

Non-small cell lung cancer (NSCLC) is one of the most common and fatal cancers in the world. Circular RNA (circRNA) can broadly participate in the initiation and progression of the NSCLC. However, the regulatory mechanisms of circRNA in NSCLC remain poorly understood. In present study, we aimed to explore the potential role of circ_0101675 in the progression of NSCLC. Quantitative real-time polymerase chain reaction was performed to examine the expression of circ_0101675, microRNA-607 (miR-607) and programmed cell death receptor ligand 1 (PDL1) in NSCLC tissues and cells. Cell count kit 8 assay, colony formation assay, wound healing assay, transwell assay, tube formation assay and flow cytometry were applied to examine NSCLC cell proliferation, migration, invasion, angiogenesis and apoptosis. NSCLC cells were co-cultured with peripheral blood mononuclear cells to assess immune response. The protein levels of PDL1 and proteins related to apoptosis were detected by western blotting. Dual-luciferase reporter assay and RNA immunoprecipitation assay were conducted to verify the direct target site between miR-607 and circ_0101675 or PDL1. The experiments in vivo were employed to explore the effects of circ_0101675 on tumor growth in NSCLC. Circ_0101675 and PDL1 were high-expressed, while miR-607 was low-expressed in NSCLC cells and cancer tissues. The suppression of circ_0101675 suppressed growth, migration, invasion, angiogenesis and immune escape in NSCLC cells. Mechanistically, we found that high level of circ_0101675 could upregulate PDL1 expression via sponging miR-607. Moreover, the down-regulation of circ_0101675 inhibited the growth of NSCLC tumors in vivo by enhancing miR-607 expression to decrease PDL1 expression. Taken together, our results suggested that circ_0101675 might promote the proliferation, migration, invasion, and immune evasion abilities of NSCLC through miR-607/PDL1 axis.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.