Du Zhenhua, Jia Zhili, Lin Yao, Zhao Xudong, Cao Gengsheng, Wang Hengbin
School of Life Sciences, Henan University, Kaifeng 475004, China.
Department of Obstetrics and Gynecology, Li Ka Shing Faculty of Medicine, The University ofHong Kong, Hong Kong 999077, China.
Cells. 2025 Aug 15;14(16):1262. doi: 10.3390/cells14161262.
Esophageal squamous cell carcinoma (ESCC) is a prevalent malignancy, ranking eleventh in incidence and seventh in mortality globally. Remodeling and Spacing factor 1 (RSF1), a chromatin remodeling factor, is frequently overexpressed in various tumors and correlates with poor prognosis. This study, combining public database analysis and clinical sample validation, reveals significantly elevated RSF1 expression in ESCC tumor tissues, confirmed further in an ESCC orthotopic model. Functional assays show that RSF1 knockout (KO) significantly inhibits ESCC cell proliferation, migration, invasion, and in vivo tumor growth, while reintroducing RSF1 restores its oncogenic effects. Proteomic analysis highlights that RSF1 KO disrupts pathways associated with cell cycle control, apoptosis, and focal adhesion. Experimentally, RSF1 KO induces apoptosis and G2/M arrest, establishing its essential role in ESCC progression. Collectively, these findings establish RSF1 as an oncogenic driver and a promising therapeutic target in ESCC.
食管鳞状细胞癌(ESCC)是一种常见的恶性肿瘤,在全球发病率中排名第十一,死亡率中排名第七。重塑与间隔因子1(RSF1)是一种染色质重塑因子,在各种肿瘤中经常过度表达,且与预后不良相关。本研究结合公共数据库分析和临床样本验证,揭示了ESCC肿瘤组织中RSF1表达显著升高,并在ESCC原位模型中进一步得到证实。功能实验表明,RSF1基因敲除(KO)显著抑制ESCC细胞增殖、迁移、侵袭以及体内肿瘤生长,而重新引入RSF1可恢复其致癌作用。蛋白质组学分析突出显示,RSF1基因敲除会破坏与细胞周期控制、细胞凋亡和粘着斑相关的信号通路。实验表明,RSF1基因敲除可诱导细胞凋亡和G2/M期阻滞,确立了其在ESCC进展中的重要作用。总之,这些发现确立了RSF1作为ESCC致癌驱动因素和有前景的治疗靶点的地位。