TP53 缺失通过上调 NF-κB-IFN-β-MHC-Ia 信号促进骨肉瘤对 NK 细胞的抵抗
TP53 Loss Elevates NF-κB-IFN-β-MHC-Ia Signaling to Promote NK Cell Resistance in Osteosarcoma.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:An overview of kinin mediated events in cancer progression and therapeutic applications.
An overview of kinin mediated events in cancer progression and therapeutic applications.
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激肽是在组织微环境炎症状态中产生的生物活性肽,参与癌症进展和炎症反应。激肽通过激活两种G蛋白偶联受体传递信号:可诱导的缓激肽B1受体(B1R)和组成型受体B2(B2R)。激肽受体活化并与受体酪氨酸激酶发生交叉调控后,可激活ERK/MAPK、PI3K、PKC和p38等多条信号通路,调节癌症标志性特征。激肽介导过程发生扰动与癌症侵袭、基质重塑和转移的多个方面相关。在肿瘤微环境中,激肽可启动成纤维细胞活化、与间充质干细胞相互作用并募集免疫细胞。尽管激肽在转移和肿瘤微环境中的确切作用尚未完全明确,多种激肽受体拮抗剂已显示抗转移潜力。本文综述激肽复杂的生物学特性及其在癌症发病机制和治疗方面的作用。
Kinins are bioactive peptides generated in the inflammatory milieu of the tissue microenvironment, which is involved in cancer progression and inflammatory response. Kinins signals through activation of two G-protein coupled receptors; inducible Bradykinin Receptor B1 (B1R) and constitutive receptor B2 (B2R). Activation of kinin receptors and its cross-talk with receptor tyrosine kinases activates multiple signaling pathways, including ERK/MAPK, PI3K, PKC, and p38 pathways regulating cancer hallmarks.
Perturbations of the kinin-mediated events are implicated in various aspects of cancer invasion, matrix remodeling, and metastasis. In the tumor microenvironment, kinins initiate fibroblast activation, mesenchymal stem cell interactions, and recruitment of immune cells. Albeit the precise nature of kinin function in the metastasis and tumor microenvironment are not completely clear yet, several kinin receptor antagonists show anti-metastatic potential.
Here, we showcase an overview of the complex biology of kinins and their role in cancer pathogenesis and therapeutic aspects.
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