Stomatology Department, North China University of Science and Technology Affiliated Hospital, Tangshan, China.
Braz J Med Biol Res. 2021 Mar 15;54(5):e10093. doi: 10.1590/1414-431X202010093. eCollection 2021.
The aim of this study was to explore the effect of hsa_circ_0002162 on regulating cell proliferation, apoptosis, and invasion, and investigate its potential target microRNA (miRNA) in tongue squamous cell carcinoma (TSCC). Hsa_circ_0002162 expression was detected in human TSCC cell lines and human oral keratinocytes (HOK) cell line. Cell proliferation, apoptosis, invasion, and candidate target miRNA expressions were detected in hsa_circ_0002162 knockdown-treated CAL-27 cells and hsa_circ_0002162 overexpression-treated SCC-9 cells. In the rescue experiment, miR-33a-5p knockdown plasmid was transfected into hsa_circ_0002162 knockdown-treated CAL-27 cells, while miR-33a-5p overexpression plasmid was transfected into hsa_circ_0002162 overexpression-treated SCC-9 cells. Subsequently, cell proliferation, apoptosis, and invasion were detected, and then luciferase reporter assay was performed. Hsa_circ_0002162 expression was increased in human TSCC cell lines SCC-9, CAL-27, HSC-4, and SCC-25 compared with HOK. In CAL-27 cells, hsa_circ_0002162 knockdown inhibited cell proliferation and invasion and promoted apoptosis. In SCC-9 cells, hsa_circ_0002162 overexpression enhanced cell proliferation and invasion and suppressed apoptosis. Furthermore, a negative regulation of hsa_circ_0002162 on miR-33a-5p (but not miR-302b-5p and miR-545-5p) was observed. In the rescue experiment, miR-33a-5p knockdown increased cell proliferation and invasion, and decreased apoptosis in hsa_circ_0002162 knockdown-treated CAL-27 cells, whereas miR-33a-5p overexpression decreased cell proliferation and invasion, but increased apoptosis in hsa_circ_0002162 overexpression-treated SCC-9 cells. The luciferase reporter assay showed the direct binding of hsa_circ_0002162 to miR-33a-5p. In conclusion, hsa_circ_0002162 had an important role in malignant progression of TSCC through targeting miR-33a-5p.
本研究旨在探讨 hsa_circ_0002162 对舌鳞状细胞癌（TSCC）中细胞增殖、凋亡和侵袭的调节作用，并研究其潜在的靶微小 RNA（miRNA）。检测了人 TSCC 细胞系和人口腔角质形成细胞（HOK）细胞系中 hsa_circ_0002162 的表达。在 hsa_circ_0002162 敲低处理的 CAL-27 细胞和 hsa_circ_0002162 过表达处理的 SCC-9 细胞中检测细胞增殖、凋亡、侵袭和候选靶 miRNA 的表达。在挽救实验中，将 miR-33a-5p 敲低质粒转染至 hsa_circ_0002162 敲低处理的 CAL-27 细胞中，而将 miR-33a-5p 过表达质粒转染至 hsa_circ_0002162 过表达处理的 SCC-9 细胞中。随后，检测细胞增殖、凋亡和侵袭，并进行荧光素酶报告基因检测。与 HOK 相比，hsa_circ_0002162 在人 TSCC 细胞系 SCC-9、CAL-27、HSC-4 和 SCC-25 中的表达增加。在 CAL-27 细胞中，hsa_circ_0002162 敲低抑制细胞增殖和侵袭，促进凋亡。在 SCC-9 细胞中，hsa_circ_0002162 过表达增强细胞增殖和侵袭，抑制凋亡。此外，观察到 hsa_circ_0002162 对 miR-33a-5p 的负调控（而不是 miR-302b-5p 和 miR-545-5p）。在挽救实验中，miR-33a-5p 敲低增加了 hsa_circ_0002162 敲低处理的 CAL-27 细胞中的细胞增殖和侵袭，降低了凋亡，而 miR-33a-5p 过表达降低了 hsa_circ_0002162 过表达处理的 SCC-9 细胞中的细胞增殖和侵袭，但增加了凋亡。荧光素酶报告基因检测显示 hsa_circ_0002162 与 miR-33a-5p 直接结合。总之，hsa_circ_0002162 通过靶向 miR-33a-5p 在 TSCC 的恶性进展中发挥重要作用。
