USP39 Promotes the Viability and Migration of Head and Neck Squamous Cell Carcinoma Cell by Regulating STAT1.

IF 2.7 4区 医学 Q3 ONCOLOGY Technology in Cancer Research & Treatment Pub Date : 2024-01-01 DOI:10.1177/15330338241250298
Yu Hu, Yang Wang, Wenrui Hu, Chenrui Hu, Bin Wang, Congli Liu, Anqi Deng, Bing Shen, Kaile Wu, Yehai Liu
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Abstract

Objective: Ubiquitin-specific peptidase 39 (USP39) plays a carcinogenic role in many cancers, but little research has been conducted examining whether it is involved in head and neck squamous cell carcinoma (HNSCC). Therefore, this study explored the functional role of USP39 in HNSCC. Method: Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to identify differentially expressed proteins (DEPs) between the HNSCC tumor and adjacent healthy tissues. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were used to assess the functional enrichment of DEPs. Immunohistochemistry was used to detect protein expression. The viability and migration of two HNSCC cell lines, namely CAL27 and SCC25, were detected using the cell counting kit-8 assay and a wound healing assay, respectively. Quantitative real-time PCR was used to detect the expression level of signal transducer and activator of transcription 1 (STAT1) mRNA. Results: LC-MS/MS results identified 590 DEPs between HNSCC and adjacent tissues collected from 4 patients. Through GO and KEGG pathway analyses, 34 different proteins were found to be enriched in the spliceosome pathway. The expression levels of USP39 and STAT1 were significantly higher in HNSCC tumor tissue than in adjacent healthy tissue as assessed by LC-MS/MS analysis, and the increased expression of USP39 and STAT1 protein was confirmed by immunohistochemistry in clinical samples collected from 7 additional patients with HNSCC. Knockdown of USP39 or STAT1 inhibited the viability and migration of CAL27 and SCC25 cells. In addition, USP39 knockdown inhibited the expression of STAT1 mRNA in these cells. Conclusion: Our findings indicated that USP39 knockdown may inhibit HNSCC viability and migration by suppressing STAT1 expression. The results of this study suggest that USP39 may be a potential new target for HNSCC clinical therapy or a new biomarker for HNSCC.

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USP39 通过调节 STAT1 促进头颈部鳞状细胞癌细胞的活力和迁移
目的:泛素特异性肽酶 39(USP39)在许多癌症中发挥致癌作用,但很少有研究探讨它是否参与头颈部鳞状细胞癌(HNSCC)的发病。因此,本研究探讨了 USP39 在 HNSCC 中的功能作用。方法:液相色谱-串联质谱采用液相色谱-串联质谱法(LC-MS/MS)鉴定 HNSCC 肿瘤与邻近健康组织之间的差异表达蛋白(DEPs)。基因本体(GO)和京都基因组百科全书(KEGG)通路分析用于评估 DEPs 的功能富集。免疫组织化学用于检测蛋白质表达。使用细胞计数试剂盒-8测定法和伤口愈合测定法分别检测了两种HNSCC细胞系(即CAL27和SCC25)的存活率和迁移率。采用定量实时 PCR 检测信号转导和激活转录 1(STAT1)mRNA 的表达水平。结果LC-MS/MS结果在4名患者的HNSCC和邻近组织中发现了590个DEPs。通过 GO 和 KEGG 通路分析,发现剪接体通路中富含 34 种不同的蛋白质。经 LC-MS/MS 分析评估,USP39 和 STAT1 在 HNSCC 肿瘤组织中的表达水平明显高于邻近的健康组织。敲除 USP39 或 STAT1 可抑制 CAL27 和 SCC25 细胞的活力和迁移。此外,敲除 USP39 还抑制了 STAT1 mRNA 在这些细胞中的表达。结论我们的研究结果表明,敲除 USP39 可通过抑制 STAT1 的表达来抑制 HNSCC 的活力和迁移。本研究结果表明,USP39 可能是 HNSCC 临床治疗的潜在新靶点或 HNSCC 的新生物标记物。
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来源期刊
CiteScore
4.40
自引率
0.00%
发文量
202
审稿时长
2 months
期刊介绍: Technology in Cancer Research & Treatment (TCRT) is a JCR-ranked, broad-spectrum, open access, peer-reviewed publication whose aim is to provide researchers and clinicians with a platform to share and discuss developments in the prevention, diagnosis, treatment, and monitoring of cancer.
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