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SP2 诱导的 circPUM1 调控口腔鳞状细胞癌化疗耐药与 NK 细胞毒性

英文原题:SP2-induced circPUM1 modulates chemoresistance and nature killer cell toxicity in oral squamous cell carcinoma.

查看英文原题

SP2-induced circPUM1 modulates chemoresistance and nature killer cell toxicity in oral squamous cell carcinoma.

PubMed 2023/08/09(内容时间) J Cell Mol Med Q2 · IF 4.7(JCR 2025)

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中文摘要

口腔鳞状细胞癌(OSCC)是一种发生于口腔的肿瘤,其特征是分化及向淋巴结转移。尽管近年来诊断策略和临床治疗有所改善,但 OSCC 患者的预后仍不理想。

本研究验证了 circPUM1 在 OSCC 细胞中的特征,随后构建了 circPUM1 失调的细胞模型,显示 circPUM1 促进化疗耐药和自然杀伤(NK)细胞毒性。

此外,转录因子 SP2 调控 OSCC 细胞中 circPUM1 的表达,circPUM1 作为 miR-770-5p 的分子海绵。而且,Nucleosome Assembly Protein 1 Like 1(NAP1L1)是 miR-770-5p 的下游靶点,并且对于 circPUM1 介导的 OSCC 细胞顺铂耐药和 NK 细胞毒性至关重要。由 SP2、circPUM1、miR-770-5p 和 NAP1L1 组成的网络在 OSCC 中似乎为开发诊断或治疗 OSCC 的新靶点提供了一条有前景的途径。

展开英文摘要原文

Oral squamous cell carcinoma (OSCC) is a type of tumour found in the cavity that is characterized by differentiation and metastasis to the lymph nodes. Although diagnosis strategy and clinical treatment have recently improved, the outcomes for OSCC patients remain unsatisfactory.

This study verified the characteristics of circPUM1 in OSCC cells, subsequently generating dysregulated circPUM1 cell models, showing that circPUM1 promoted chemoresistance and natural killer (NK) cell toxicity.

Furthermore, the transcription factor SP2 regulated the expression of circPUM1 in OSCC cells, circPUM1 acted as a molecular sponge for miR-770-5p.

Moreover, Nucleosome Assembly Protein 1 Like 1 (NAP1L1) is a downstream target for miR-770-5p and essential for circPUM1-mediated cisplatin resistance and NK cell cytotoxicity in OSCC cells. The network composed of SP2, circPUM1, miR-770-5p and NAP1L1 in OSCC appears to be a promising avenue for the development of novel targets for diagnosing or treating OSCC.

论文信息

作者
Liu L、Zou C、Lv X、Wei H、Wu S、Song J、Tang Z、Luo H
单位
Foshan Stomatological Hospital, School of Medicine, Foshan University, Foshan, China.China
文献类型
非美国政府资助研究
期刊
Journal of cellular and molecular medicine2024 Mar
原文标识
PubMed 37556099 · DOI 10.1111/jcmm.17888