活化信号转导和转录激活因子 2 蛋白抑制剂是口腔鳞状细胞癌的一种肿瘤蛋白,与吸烟有关 - 一项体外研究

IF 3.4 3区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Journal of Dental Sciences Pub Date : 2024-07-20 DOI:10.1016/j.jds.2024.07.013
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引用次数: 0

摘要

背景/目的口腔癌是台湾最常见的恶性肿瘤之一。由于口腔癌细胞的异质性,患者的五年存活率仅为 50%。翻译后修饰导致蛋白质的多样性,并直接影响细胞功能。材料与方法分别用PIAS2表达载体转染细胞或用siRNA敲除低表达和高表达的PIAS2,从而调节PIAS2的表达。对这些细胞进行侵袭、迁移和增殖试验,以评估 PIAS2 的影响。还检测了基因型的变化,如上皮-间质转化(EMT)标记物。此外,还研究了香烟冷凝物(CSC)对口腔鳞状细胞癌(OSCC)细胞中 PIAS2 表达的影响。在 PIAS2 低表达的 YD38 和 SAS 细胞中,PIAS2 的过表达增强了细胞的增殖、侵袭和迁移。PIAS2 的过表达也会影响 EMT 基因的表达,抑制 E-cadherin 的表达,增加纤维连接蛋白的表达。相反,在 OECM1 和 SCC25 细胞中敲除 PIAS2 可抑制恶性行为并逆转 EMT 标记,增加 E 角连蛋白,减少纤维连接蛋白的表达。结论PIAS2是口腔癌的致癌基因,吸烟会诱导PIAS2的表达。PIAS2水平的升高会导致口腔癌恶性程度的增强。
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Protein inhibitor of activated signal transducer and activator of transcription 2 is an oncoprotein in oral squamous cell carcinoma and related to cigarette smoking - An in vitro study

Background/purpose

Oral cancer is one of the most prevalent malignant tumors in Taiwan. Due to the heterogeneity of oral cancer cells, the five-year survival rate of patients is only 50%. Post-translational modifications contribute to protein diversity and directly influence cell functions. The protein inhibitor of activated signal transducer and activator of transcription 2 (PIAS2) is known to undergo post-translational modifications, yet its impact on oral cancer remains unclear.

Materials and methods

PIAS2 expression was modulated by transfecting cells with a PIAS2 expression vector or by knocking down PIAS2 using siRNA with low and high PIAS2 expression, respectively. These cells were subjected to invasion, migration, and proliferation assays to evaluate the effects of PIAS2. Changes in genotype, such as epithelial-mesenchymal transition (EMT) markers, were also examined. Additionally, the effect of cigarette smoke condensate (CSC) on PIAS2 expression in oral squamous cell carcinoma (OSCC) cells was investigated.

Results

Overexpression of PIAS2 significantly increased the malignant behaviors of oral cancer cells. In YD38 and SAS cells with low PIAS2 expression, overexpression of PIAS2 enhanced proliferation, invasion, and migration. PIAS2 overexpression also affected EMT gene expression, suppressing E-cadherin and increasing fibronectin expression. Conversely, PIAS2 knockdown in OECM1 and SCC25 cells suppressed malignant behaviors and reversed EMT markers, increasing E-cadherin and decreasing fibronectin expression. Furthermore, a dose-dependent increase in PIAS2 expression was observed when OSCC cells were treated with CSC.

Conclusion

PIAS2 functions as an oncogene in oral cancer, and cigarette smoking induces PIAS2 expression. Increased PIAS2 levels lead to enhanced malignancy in oral cancer.

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来源期刊
Journal of Dental Sciences
Journal of Dental Sciences 医学-牙科与口腔外科
CiteScore
5.10
自引率
14.30%
发文量
348
审稿时长
6 days
期刊介绍: he Journal of Dental Sciences (JDS), published quarterly, is the official and open access publication of the Association for Dental Sciences of the Republic of China (ADS-ROC). The precedent journal of the JDS is the Chinese Dental Journal (CDJ) which had already been covered by MEDLINE in 1988. As the CDJ continued to prove its importance in the region, the ADS-ROC decided to move to the international community by publishing an English journal. Hence, the birth of the JDS in 2006. The JDS is indexed in the SCI Expanded since 2008. It is also indexed in Scopus, and EMCare, ScienceDirect, SIIC Data Bases. The topics covered by the JDS include all fields of basic and clinical dentistry. Some manuscripts focusing on the study of certain endemic diseases such as dental caries and periodontal diseases in particular regions of any country as well as oral pre-cancers, oral cancers, and oral submucous fibrosis related to betel nut chewing habit are also considered for publication. Besides, the JDS also publishes articles about the efficacy of a new treatment modality on oral verrucous hyperplasia or early oral squamous cell carcinoma.
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