Focal adhesion kinase-mediated interaction between tumor and immune cells in the tumor microenvironment: implications for cancer-associated therapies and tumor progression

Louis Boafo Kwantwi, Theophilus Tandoh
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Abstract

Focal adhesion kinase (FAK) expression has been linked to tumor growth, immunosuppression, metastasis, angiogenesis, and therapeutic resistance through kinase-dependent and kinase scaffolding functions in the nucleus and cytoplasm. Hence, targeting FAK alone or with other agents has gained attention as a potential therapeutic strategy. Moreover, mounting evidence shows that FAK activity can influence the tumor immune microenvironment crosstalk to support tumor progression. Recently, tumor immune microenvironment interaction orchestrators have shown to be promising therapeutic agents for cancer immunotherapies. Therefore, this review highlights how FAK regulates the tumor immune microenvironment interplay to promote tumor immune evasive mechanisms and their potential for combination therapies with standard cancer treatments.

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肿瘤微环境中肿瘤和免疫细胞之间由病灶粘附激酶介导的相互作用:对癌症相关疗法和肿瘤进展的影响
病灶粘附激酶(FAK)的表达与肿瘤生长、免疫抑制、转移、血管生成和治疗耐药性有关,它在细胞核和细胞质中起着激酶依赖和激酶支架的作用。因此,单独或与其他药物一起靶向 FAK 作为一种潜在的治疗策略受到了关注。此外,越来越多的证据表明,FAK 的活性可影响肿瘤免疫微环境的串联,从而支持肿瘤的进展。最近,肿瘤免疫微环境相互作用协调者已被证明是有希望用于癌症免疫疗法的治疗药物。因此,本综述将重点介绍 FAK 如何调控肿瘤免疫微环境的相互作用以促进肿瘤免疫规避机制,以及它们与标准癌症疗法联合治疗的潜力。
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