32 种癌症类型中整合素家族的综合特征。

Cheng Zou, Jinwei Zhu, Jiangling Xiong, Yu Tian, Yousong Peng, Edwin Cheung, Dingxiao Zhang
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摘要

整合素基因广泛参与肿瘤发生。然而,目前还缺乏对整合素家族成员及其相互作用组在泛癌症水平上的全面描述。在这里,我们系统分析了 32 种癌症类型中约 10,000 个肿瘤中的整合素家族。在全球范围内,整合素是一种经常发生改变和表达失调的通路,其改变和失调总体上具有原发肿瘤性。整合素家族的表达失调比突变情况更能成功地识别出具有高度增殖和干性的侵袭性肿瘤亚群。研究结果表明,有几种分子机制共同调节整合素的表达,其方式取决于具体情况。为了实现潜在的临床应用,我们构建了一个加权评分系统--integrinScore,用于测量单个肿瘤的整合素信号转导模式。值得注意的是,整合素分数与多种癌症的预定义分子亚型一致相关,整合素分数高的肿瘤更具侵袭性。重要的是,整合素分数与肿瘤的增殖、干性、肿瘤微环境、转移和免疫特征密切相关。整合素分数还能预测患者对免疫疗法的反应。通过挖掘药物数据库,我们发现了一系列可能调节整合素信号转导的化合物。最后,我们建立了一个用户友好型数据库--泛癌症整合素探索者(PIExplorer)(http://computationalbiology.cn/PIExplorer),方便研究人员探索整合素相关知识。总之,我们提供了癌症中整合素的全面特征,并为开发整合素靶向疗法提供了基因特异性和癌症特异性依据。
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Comprehensive Characterization of the Integrin Family Across 32 Cancer Types.

Integrin genes are widely involved in tumorigenesis. Yet, a comprehensive characterization of integrin family members and their interactome at the pan-cancer level is lacking. Here, we systematically analyzed integrin family in approximately 10,000 tumors across 32 cancer types. Globally, integrins represent a frequently altered and misexpressed pathway, with alteration and dysregulation overall being protumorigenic. Expression dysregulation, better than mutational landscape, of integrin family successfully identifies a subgroup of aggressive tumors with a high level of proliferation and stemness. The results reveal that several molecular mechanisms collectively regulate integrin expression in a context-dependent manner. For potential clinical usage, we constructed a weighted scoring system, integrinScore, to measure integrin signaling patterns in individual tumors. Remarkably, integrinScore was consistently correlated with predefined molecular subtypes in multiple cancers, with integrinScore-high tumors being more aggressive. Importantly, integrinScore was cancer-dependent and closely associated with proliferation, stemness, tumor microenvironment, metastasis, and immune signatures. IntegrinScore also predicted patients' response to immunotherapy. By mining drug databases, we unraveled an array of compounds that may modulate integrin signaling. Finally, we built a user-friendly database, Pan-cancer Integrin Explorer (PIExplorer; http://computationalbiology.cn/PIExplorer), to facilitate researchers to explore integrin-related knowledge. Collectively, we provide a comprehensive characterization of integrins across cancers and offer gene-specific and cancer-specific rationales for developing integrin-targeted therapy.

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