PDF(Pubmed)
Abstract：
Cyclin-Dependent Kinase 16 (CDK16) plays significant biological roles in various diseases. Nonetheless, its function in different cancer types and its relationship with the Tumor Immune Microenvironment (TIME) are still not well-understood.
We analyzed the expression profile, genetic alterations, clinical features, and prognostic value of CDK16 in pan-cancer using data from The Cancer Genome Atlas, Genotype-Tissue Expression databases, and in vitro experiments. Additionally, the TIMER2 and ImmuCellAI databases were utilized to assess the correlation between CDK16 expression and immune cell infiltration levels. Finally, we examined the correlation between CDK16 and the response to immunotherapy using collected immunotherapy data.
CDK16 is notably overexpressed in pan-cancer and is a risk factor for poor prognosis in various cancers. Our findings reveal that CDK16 regulates not only cell cycle-related functions to promote cell proliferation but also the autoimmunity-related functions of the innate and adaptive immune systems, along with other immune-related signaling pathways. Moreover, CDK16 overexpression contributes to an immunosuppressive tumor microenvironment, extensively suppressing immune-related features such as the expression of immune-related genes and pathways, as well as the count of immune-infiltrating cells. Our analysis indicated that individuals with low CDK16 expression showed higher response rates to immune checkpoint inhibitors and longer overall survival compared to those with high CDK16 expression.
This study establishes CDK16 as a potential biomarker for predicting poor prognosis in a wide range of cancers. Its role in shaping the immunosuppressive tumor microenvironment and influencing the efficacy of immunotherapy highlights the urgent need for developing targeted therapies against CDK16, offering new avenues for cancer treatment and management.
We analyzed the expression profile, genetic alterations, clinical features, and prognostic value of CDK16 in pan-cancer using data from The Cancer Genome Atlas, Genotype-Tissue Expression databases, and in vitro experiments. Additionally, the TIMER2 and ImmuCellAI databases were utilized to assess the correlation between CDK16 expression and immune cell infiltration levels. Finally, we examined the correlation between CDK16 and the response to immunotherapy using collected immunotherapy data.
CDK16 is notably overexpressed in pan-cancer and is a risk factor for poor prognosis in various cancers. Our findings reveal that CDK16 regulates not only cell cycle-related functions to promote cell proliferation but also the autoimmunity-related functions of the innate and adaptive immune systems, along with other immune-related signaling pathways. Moreover, CDK16 overexpression contributes to an immunosuppressive tumor microenvironment, extensively suppressing immune-related features such as the expression of immune-related genes and pathways, as well as the count of immune-infiltrating cells. Our analysis indicated that individuals with low CDK16 expression showed higher response rates to immune checkpoint inhibitors and longer overall survival compared to those with high CDK16 expression.
This study establishes CDK16 as a potential biomarker for predicting poor prognosis in a wide range of cancers. Its role in shaping the immunosuppressive tumor microenvironment and influencing the efficacy of immunotherapy highlights the urgent need for developing targeted therapies against CDK16, offering new avenues for cancer treatment and management.
摘要：
背景：细胞周期蛋白依赖性激酶16（CDK16）在各种疾病中起着重要的生物学作用。尽管如此，其在不同癌症类型中的功能及其与肿瘤免疫微环境（TIME）的关系仍未得到很好的理解。
方法：我们分析了表达谱，遗传改变,临床特征,使用来自癌症基因组图谱的数据，以及CDK16在泛癌症中的预后价值，基因型-组织表达数据库,和体外实验。此外,我们利用TIMER2和ImmuCellAI数据库评估CDK16表达与免疫细胞浸润水平之间的相关性.最后,我们使用收集的免疫疗法数据检查了CDK16与免疫疗法应答之间的相关性.
结果：CDK16在泛癌症中明显过表达，是各种癌症预后不良的危险因素。我们的发现表明，CDK16不仅调节细胞周期相关功能以促进细胞增殖，而且还调节先天和适应性免疫系统的自身免疫相关功能。以及其他免疫相关的信号通路。此外，CDK16过表达有助于免疫抑制肿瘤微环境，广泛抑制免疫相关特征，如免疫相关基因和途径的表达，以及免疫浸润细胞的计数。我们的分析表明，与具有高CDK16表达的个体相比，具有低CDK16表达的个体对免疫检查点抑制剂的反应率更高，总体生存期更长。
结论：本研究确立了CDK16作为预测多种癌症预后不良的潜在生物标志物。它在塑造免疫抑制肿瘤微环境和影响免疫疗法疗效方面的作用突出了开发针对CDK16的靶向疗法的迫切需要，为癌症治疗和管理提供了新的途径。
方法：我们分析了表达谱，遗传改变,临床特征,使用来自癌症基因组图谱的数据，以及CDK16在泛癌症中的预后价值，基因型-组织表达数据库,和体外实验。此外,我们利用TIMER2和ImmuCellAI数据库评估CDK16表达与免疫细胞浸润水平之间的相关性.最后,我们使用收集的免疫疗法数据检查了CDK16与免疫疗法应答之间的相关性.
结果：CDK16在泛癌症中明显过表达，是各种癌症预后不良的危险因素。我们的发现表明，CDK16不仅调节细胞周期相关功能以促进细胞增殖，而且还调节先天和适应性免疫系统的自身免疫相关功能。以及其他免疫相关的信号通路。此外，CDK16过表达有助于免疫抑制肿瘤微环境，广泛抑制免疫相关特征，如免疫相关基因和途径的表达，以及免疫浸润细胞的计数。我们的分析表明，与具有高CDK16表达的个体相比，具有低CDK16表达的个体对免疫检查点抑制剂的反应率更高，总体生存期更长。
结论：本研究确立了CDK16作为预测多种癌症预后不良的潜在生物标志物。它在塑造免疫抑制肿瘤微环境和影响免疫疗法疗效方面的作用突出了开发针对CDK16的靶向疗法的迫切需要，为癌症治疗和管理提供了新的途径。
