Dept. of Stomatology, Affiliated Hospital of Weifang Medical University, Weifang 261000, China.
School of Stomatology, Weifang Medical University, Weifang 261053, China.
Hua Xi Kou Qiang Yi Xue Za Zhi. 2024 Feb 1;42(1):46-55. doi: 10.7518/hxkq.2024.2023237.
This study aimed to explore the effect of pituitary tumor-transforming gene 1 (PTT-G1) on the invasion and proliferation of oral squamous cell carcinoma (OSCC) cell lines under the action of miR-362-3p.
The bioinformatics online database was used to query the expression of PTTG1 in head and neck squamous cell carcinoma (HNSCC). The expression of PTTG1 in the Cal-27, HN-30, and HOK cell lines was detected by Western blot. A wound-healing assay was used to determine the effect of PTTG1 on the migration ability of the OSCC cells. The Transwell assay was used to examine the changes in cell-invasion ability. 5-ethynyl-2'-deoxyuridine (EdU) cell-proliferation assay was used to detect changes in cell-proliferation ability. Bioinformatics approach predicted the upstream miRNA of PTTG1. The targeting relationship between miR-362-3p and PTTG1 was examined by the dual luciferase assay, and quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression of miRNA in OSCC tissues.
The ENCORI database showed that PTTG1 expression was up-regulated in OSCC tissues. Western blot confirmed that PTTG1 expression was up-regulated in Cal-27 and HN-30 cells than HOK cells. PTTG1 knockout can inhibit the migration, invasion, and proliferation of Cal-27 and HN-30 cells (<0.05). Bioinformatics prediction websites predicted that the upstream miRNA of PTTG1 was miR-362-3p, and PTTG1 can bind to miR-362-3p. Results of qRT-PCR showed that miR-362-3p expression was downregulated in OSCC tissues compared with normal tissue (<0.05). Transwell and EdU experiments confirmed that miR-362-3p knockdown can promote the invasion and proliferation of Cal-27 and HN-30 after PTTG1 knockdown.
miR-362-3p can inhibit the invasion and proliferation of Cal-27 and HN-30 cells by targeting PTTG1.
本研究旨在探讨垂体肿瘤转化基因 1(PTTG1)在 miR-362-3p 作用下对口腔鳞状细胞癌细胞系侵袭和增殖的影响。
利用生物信息学在线数据库查询头颈部鳞状细胞癌(HNSCC)中 PTTG1 的表达情况。采用 Western blot 检测 Cal-27、HN-30 和 HOK 细胞系中 PTTG1 的表达。通过划痕实验测定 PTTG1 对 OSCC 细胞迁移能力的影响。Transwell 实验检测细胞侵袭能力的变化。5-乙炔基-2'-脱氧尿苷(EdU)细胞增殖实验检测细胞增殖能力的变化。生物信息学方法预测 PTTG1 的上游 miRNA。通过双荧光素酶报告基因实验检测 miR-362-3p 与 PTTG1 的靶向关系,并用定量实时聚合酶链反应(qRT-PCR)检测 OSCC 组织中 miRNA 的表达。
ENCORI 数据库显示 PTTG1 在 OSCC 组织中表达上调。Western blot 证实 PTTG1 在 Cal-27 和 HN-30 细胞中的表达高于 HOK 细胞。PTTG1 敲除可抑制 Cal-27 和 HN-30 细胞的迁移、侵袭和增殖(<0.05)。生物信息学预测网站预测 PTTG1 的上游 miRNA 是 miR-362-3p,PTTG1 可以与 miR-362-3p 结合。qRT-PCR 结果显示,与正常组织相比,OSCC 组织中 miR-362-3p 的表达下调(<0.05)。Transwell 和 EdU 实验证实,PTTG1 敲除后 miR-362-3p 表达下调可促进 Cal-27 和 HN-30 侵袭和增殖。
miR-362-3p 可通过靶向 PTTG1 抑制 Cal-27 和 HN-30 细胞的侵袭和增殖。