RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:"Targeting platelets in breast cancer: Insights into pathophysiology and therapeutic strategies".
"Targeting platelets in breast cancer: Insights into pathophysiology and therapeutic strategies".
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乳腺癌细胞与血小板建立复杂的相互作用,导致血小板活化并转化为支持肿瘤生长和进展的细胞。活化血小板通过分泌生物活性因子,包括 TGF-β、VEGF 和 PDGF,促进癌细胞增殖、血管生成和转移。通过多种信号通路,活化血小板加速上皮-间质转化(EMT)和肿瘤细胞血管内渗。它们还保护循环肿瘤细胞,并通过抑制自然杀伤(NK)细胞,促进免疫逃逸和向转移靶组织的浸润。此外,血小板释放多种因子,为转移微环境做准备并支持远处部位的克隆扩增。鉴于血小板在乳腺癌进展多个阶段中的促进作用,它们代表了靶向治疗和向癌细胞递送药物的有前景的靶点。在本综述中,我们详细呈现了血小板在乳腺癌进展不同阶段中的作用,并阐述了在癌症治疗中靶向它们的新兴策略。
Breast cancer cells establish complex interactions with platelets, leading to platelet activation and their transformation into cells that support tumor growth and progression. Activated platelets promote cancer cell proliferation, angiogenesis, and metastasis through the secretion of bioactive factors, including TGF-β, VEGF, and PDGF.
Through multiple signaling pathways, activated platelets accelerate epithelial-mesenchymal transition (EMT) and tumor cell intravasation. They also protect circulating tumor cells and, by inhibiting natural killer (NK) cells, facilitate immune evasion and infiltration into metastatic target tissues.
Furthermore, platelets release various factors that prepare the metastatic niche and support clonal expansion at distant sites. Given their facilitating roles at multiple stages of breast cancer progression, platelets represent promising targets for targeted therapies and drug delivery to cancer cells. In this Review, we present a detailed picture of the roles of platelets at different stages of breast cancer progression and illustrate emerging strategies for targeting them in cancer therapy.
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