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TP53基因的截短突变促进舌鳞状细胞癌的化疗耐药性。

A Truncated Mutation of TP53 Promotes Chemoresistance in Tongue Squamous Cell Carcinoma.

作者信息

Du Xiaoyun, Zheng Junheng, Lu Xiangwan, Zhang Yan

机构信息

MOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, China.

出版信息

Int J Mol Sci. 2025 Mar 6;26(5):2353. doi: 10.3390/ijms26052353.

Abstract

Tongue squamous cell carcinoma (TSCC), a subtype of head and neck squamous cell carcinoma, is characterized by frequent chemoresistance. Genetic mutations commonly observed in TSCC play a critical role in malignant progression; thus, elucidating their functional significance is essential for developing effective treatment strategies. To more accurately investigate the relationship between mutations and chemoresistance, we established low-passage TSCC cells, CTSC-1, obtained from a chemoresistant patient, and CTSC-2, from a treatment-naïve patient. Sanger sequencing revealed a specific TP53 mutation (Q331*) in CTSC-1, leading to the loss of the tetramerization and C-terminal regulatory domains. Notably, CTSC-1 cells harboring TP53-Q331* and CTSC-2 cells with TP53 knockout that have been engineered to ectopically express TP53-Q331* exhibit enhanced chemoresistance and increased cancer stem cell-like properties. Mechanistically, TP53-Q331* upregulates the expression of inhibitor of DNA binding 2 (ID2), which is crucial for maintaining the stemness of TSCC cells. Subsequently, ID2 activates the expression of nucleotide excision repair (NER) pathway-related genes ERCC4 and ERCC8, thereby enhancing the chemoresistance in TSCC. In conclusion, our study demonstrates that the TP53-Q331* mutation enhances TSCC chemoresistance through an ID2-mediated NER pathway, providing a potential prognostic marker and therapeutic target for TSCC chemotherapy resistance.

摘要

舌鳞状细胞癌(TSCC)是头颈部鳞状细胞癌的一种亚型,其特点是常出现化疗耐药。TSCC中常见的基因突变在恶性进展中起关键作用;因此,阐明其功能意义对于制定有效的治疗策略至关重要。为了更准确地研究突变与化疗耐药之间的关系,我们建立了低传代TSCC细胞系,从一名化疗耐药患者获取的CTSC-1,以及从一名未经治疗的患者获取的CTSC-2。桑格测序显示CTSC-1中存在一个特定的TP53突变(Q331*),导致四聚化和C端调节结构域缺失。值得注意的是,携带TP53-Q331的CTSC-1细胞以及经过基因工程改造以异位表达TP53-Q331的TP53基因敲除的CTSC-2细胞表现出增强的化疗耐药性和增加的癌症干细胞样特性。机制上,TP53-Q331上调DNA结合抑制因子2(ID2)的表达,这对于维持TSCC细胞的干性至关重要。随后,ID2激活核苷酸切除修复(NER)途径相关基因ERCC4和ERCC8的表达,从而增强TSCC的化疗耐药性。总之,我们的研究表明TP53-Q331突变通过ID2介导的NER途径增强TSCC化疗耐药性,为TSCC化疗耐药提供了一个潜在的预后标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9a8/11900931/9be888213562/ijms-26-02353-g001.jpg

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