Department of Otolaryngology-Head and Neck Surgery, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 116 South Zhuodaoquan Road, Hongshan District, Wuhan, 430079, Hubei, China.
J Mol Histol. 2022 Apr;53(2):159-171. doi: 10.1007/s10735-022-10061-1. Epub 2022 Feb 10.
The aim of our study was to illustrate the role of circular RNA 0120175 (circ_0120175) and its associated mechanism in laryngeal squamous cell carcinoma (LSCC) development. The abundance of circ_0120175, microRNA-330-3p (miR-330-3p) and solute carrier family 7, membrane 11 (SLC7A11) messenger RNA and protein was measured by quantitative real time polymerase chain reaction and Western blot assay. Cell proliferation, apoptosis, migration and invasion were assessed by cell counting kit-8 assay, flow cytometry and transwell migration and invasion assays, respectively. The interaction between miR-330-3p and circ_0120175 or SLC7A11 was confirmed by dual-luciferase reporter assay. Murine xenograft model was established to test the function of circ_0120175 in tumor growth in vivo. Circ_0120175 abundance was aberrantly increased in LSCC tissues and cell lines, and LSCC patients with high level of circ_0120175 were associated with advanced tumor staging, lymph node metastasis and short survival time. Circ_0120175 interference suppressed cell proliferation, migration and invasion and induced cell apoptosis of LSCC cells. Circ_0120175 could sponge and negatively regulate miR-330-3p expression in LSCC cells. The addition of anti-miR-330-3p partly reversed circ_0120175 knockdown-induced effects in LSCC cells. SLC7A11 bound to miR-330-3p. Circ_0120175 enhanced the abundance of SLC7A11 through sponging miR-330-3p in LSCC cells. Circ_0120175 silencing-mediated influences in LSCC cells were partly counteracted by the overexpression of SLC7A11. Circ_0120175 interference notably suppressed xenograft tumor growth in vivo. Circ_0120175 promoted proliferation, migration and invasion while impeded cell apoptosis of LSCC cells through miR-330-3p/SLC7A11 axis, which provided novel therapeutic targets for LSCC.
我们的研究目的是阐明环状 RNA 0120175（circ_0120175）及其相关机制在喉鳞状细胞癌（LSCC）发展中的作用。通过实时定量聚合酶链反应和 Western blot 分析测量 circ_0120175、微小 RNA-330-3p（miR-330-3p）和溶质载体家族 7、膜 11（SLC7A11）信使 RNA 和蛋白的丰度。通过细胞计数试剂盒-8 测定、流式细胞术和 Transwell 迁移和侵袭测定分别评估细胞增殖、凋亡、迁移和侵袭。通过双荧光素酶报告基因测定证实 miR-330-3p 与 circ_0120175 或 SLC7A11 之间的相互作用。建立了小鼠异种移植模型以测试 circ_0120175 在体内肿瘤生长中的功能。Circ_0120175 在 LSCC 组织和细胞系中异常增加，LSCC 患者高水平的 circ_0120175 与晚期肿瘤分期、淋巴结转移和短生存时间有关。Circ_0120175 干扰抑制 LSCC 细胞的增殖、迁移和侵袭，并诱导细胞凋亡。Circ_0120175 可在 LSCC 细胞中吸附并负调控 miR-330-3p 的表达。抗 miR-330-3p 的添加部分逆转了 LSCC 细胞中 circ_0120175 敲低诱导的作用。SLC7A11 与 miR-330-3p 结合。Circ_0120175 通过在 LSCC 细胞中吸附 miR-330-3p 来增强 SLC7A11 的丰度。Circ_0120175 沉默介导的 LSCC 细胞的影响部分被 SLC7A11 的过表达抵消。Circ_0120175 干扰显著抑制体内异种移植肿瘤的生长。Circ_0120175 通过 miR-330-3p/SLC7A11 轴促进 LSCC 细胞的增殖、迁移和侵袭，同时抑制细胞凋亡，为 LSCC 提供了新的治疗靶点。
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