Department of Surgery, Austin Precinct, The University of Melbourne, 145 Studley Rd, Heidelberg, VIC 3084, Australia.
Department of Hepatopancreatic-Biliary Surgery, Austin Health, 145 Studley Rd, Heidelberg, VIC 3084, Australia.
Cells. 2023 Nov 23;12(23):2692. doi: 10.3390/cells12232692.
Angiogenesis has been associated with numbers of solid tumours. Anti-angiogenesis drugs starve tumours of nutrients and oxygen but also make it difficult for a chemo reagent to distribute into a tumour, leading to aggressive tumour growth. Anti-angiogenesis drugs do not appear to improve the overall survival rate of pancreatic cancer. Vessel normalisation is merging as one of the new approaches for halting tumour progression by facilitating the tumour infiltration of immune cells and the delivery of chemo reagents. Targeting p21-activated kinases (PAKs) in cancer has been shown to inhibit cancer cell growth and improve the efficacy of chemotherapy. Inhibition of PAK enhances anti-tumour immunity and stimulates the efficacy of immune checkpoint blockades. Inhibition of PAK also improves Car-T immunotherapy by reprogramming the vascular microenvironment. This review summarizes current research on PAK's role in tumour vasculature and therapeutical response, with a focus on pancreatic cancer.
血管生成与许多实体瘤有关。抗血管生成药物会使肿瘤缺乏营养和氧气，但也会使化疗药物难以扩散到肿瘤中，从而导致肿瘤的侵袭性生长。抗血管生成药物似乎并不能提高胰腺癌的总生存率。血管正常化正成为阻止肿瘤进展的新方法之一，它可以促进免疫细胞浸润肿瘤和化疗药物的输送。研究表明，靶向癌症中的 p21 激活激酶 (PAKs) 可以抑制癌细胞生长，提高化疗效果。抑制 PAK 可以增强抗肿瘤免疫并刺激免疫检查点阻断的疗效。抑制 PAK 还可以通过重新编程血管微环境来改善 Car-T 免疫疗法。本综述总结了 PAK 在肿瘤血管生成和治疗反应中的作用的最新研究，重点是胰腺癌。
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