ArticleCell communication and signaling : CCS2024
Inhibition of P21-activated kinases 1 and 4 synergistically suppresses the growth of pancreatic cancer by stimulating anti-tumour immunity.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Article
- Rho GTPases in cancer resistance: mechanisms, vulnerabilities, and therapeutic opportunities.Biochemical Society transactions · 2026Review
- The interplay between p21-activated kinases and tumour-infiltrating dendritic cells and T cells and its implication in pancreatic cancer immunotherapy.Cell communication and signaling : CCS · 2026Review
- Knockout of PAK1 and PAK4 supresses tumour growth associated with vasculogenic mimicry inhibition through EphA2-VE-cadherin-MCAM pathway.Cell communication and signaling : CCS · 2026Article
- Targeting PAK1 or PAK4 Uncovers Different Mechanisms of Vascular Reprogramming in Pancreatic Cancer.Cells · 2025Article
- The Effects of PAK-Regulated Tumour Vasculature on Gemcitabine Response of Pancreatic Cancer.Cancers · 2025Article
- P-21 Kinase 1 or 4 Knockout Stimulated Anti-Tumour Immunity Against Pancreatic Cancer by Enhancing Vascular Normalisation.International journal of molecular sciences · 2025Article
- Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundPancreatic ductal adenocarcinoma (PDA) is one of the most lethal types of cancer, and KRAS oncogene occurs in over 90% of cases. P21-activated kinases (PAK), containing six members (PAK1 to 6), function downstream of KRAS. PAK1 and PAK4 play important roles in carcinogenesis, but their combinational effect remains unknown. In this study, we have determined the effect of dual inhibition of PAK1 and PAK4 in PDA progression using knockout (KO) cancer cell lines.
methodsMurine wild-type (WT) and PAK1KO pancreatic cancer cell lines were isolated from PAK1
resultsDouble knock out of PAK1 and PAK4 caused complete regression of tumour in a syngeneic mouse model. PAK4KO inhibited tumour growth by stimulating a rapid increase of cytotoxic CD8+ T cell infiltration. PAK1KO synergistically with PAK4KO increased cytotoxic CD8+ T cell infiltration and stimulated a sustained infiltration of CD8+ T cells at a later phase to overcome the immune evasion in the PAK4KO tumour. The human PDA tissue microarray study showed the important role of PAK1 and PAK4 in intra-tumoral T-cell function.
conclusionOur results demonstrated that dual inhibition of PAK1 and PAK4 synergistically suppressed PDA progression by stimulating cytotoxic CD8 + T cell response.
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