RFC4基因下调对口腔鳞状细胞癌细胞增殖的抑制作用。

IF 2.8 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Pengyue You, Di Wang, Zheng Liu, Shuzhen Guan, Ning Xiao, Haotian Chen, Xin Zhang, Lichuan Wu, Guizhen Wang, Haitao Dong
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引用次数: 0

摘要

口腔鳞状细胞癌(OSCC)是头颈部最常见的恶性肿瘤之一。复制因子C亚基4 (RFC4)是一种在多种人类癌症中具有活性的致癌基因,但很少在OSCC中进行研究。在本研究中,生物信息学分析发现RFC4是OSCC进展的潜在关键靶点。进一步实验表明,RFC4在OSCC肿瘤组织中的表达明显高于正常组织。RFC4的敲低导致G2/M期细胞周期阻滞,抑制体外和体内OSCC细胞的增殖。在OSCC肿瘤中,RFC4的高表达与MET水平升高、CD274和CD160水平降低有关。总的来说,本研究表明RFC4可能在OSCC肿瘤发生中起关键作用,并可作为免疫治疗疗效的潜在预测指标。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Knockdown of RFC4 inhibits cell proliferation of oral squamous cell carcinoma in vitro and in vivo.

Oral squamous cell carcinoma (OSCC) is the one of the most common types of malignant tumor found in the head and neck area. Replication factor C subunit 4 (RFC4), an oncogene active in various human cancers, has been rarely studied in OSCC. In the present study, bioinformatics analysis identified RFC4 as a potential key target in OSCC progression. Additional experiments showed that RFC4 expression was significantly higher in OSCC tumor tissues than in normal tissues. Knockdown of RFC4 led to G2/M phase cell cycle arrest and inhibited the proliferation of OSCC cells both in vitro and in vivo. High RFC4 expression in OSCC tumors was linked to increased levels of MET, along with reduced levels of CD274 and CD160. Overall, the present study reveals that RFC4 may play a pivotal role in OSCC tumorigenesis and could serve as a potential predictive marker for the efficacy of immunotherapy.

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来源期刊
FEBS Open Bio
FEBS Open Bio BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
5.10
自引率
0.00%
发文量
173
审稿时长
10 weeks
期刊介绍: FEBS Open Bio is an online-only open access journal for the rapid publication of research articles in molecular and cellular life sciences in both health and disease. The journal''s peer review process focuses on the technical soundness of papers, leaving the assessment of their impact and importance to the scientific community. FEBS Open Bio is owned by the Federation of European Biochemical Societies (FEBS), a not-for-profit organization, and is published on behalf of FEBS by FEBS Press and Wiley. Any income from the journal will be used to support scientists through fellowships, courses, travel grants, prizes and other FEBS initiatives.
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