ArticleCellular and molecular life sciences : CMLS2024
Platelet stimulation-regulated expression of ILK and ITGB3 contributes to intrahepatic cholangiocarcinoma progression through FAK/PI3K/AKT pathway activation.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Tumor-derived CTHRC1 mediates ITGB3-dependent osteoclast differentiation to promote prostate cancer bone metastasis.Oncogene · 2026Article
- AIBP deficiency drives MAFLD advancement via ITGβ3 mediated lipid metabolism disruption and pro-inflammatory activation.Cell communication and signaling : CCS · 2026Article
- Integrin β3: structural functions, tumour microenvironment regulatory roles and targeted intervention strategies.Frontiers in immunology · 2026Review
- From escort to target, the multidimensional roles and prospects of platelets in tumor immune checkpoint inhibitor therapy.Frontiers in immunology · 2026Review
- Tumor-mediated remote regulation of peripheral blood platelets.Cell biology and toxicology · 2025Review
- Integrative analysis of scRNA-seq and RNA-seq to investigate the prognostic value of lactylation and fibroblast-related genes in intrahepatic cholangiocarcinoma.Scientific reports · 2025Article
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3 authors.
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Abstract
objectiveIntrahepatic cholangiocarcinoma (iCCA) is a highly lethal hepatobiliary malignancy with an increasing incidence annually. Extensive research has elucidated the existence of a reciprocal interaction between platelets and cancer cells, which promotes tumor proliferation and metastasis. This study aims to investigate the function and mechanism underlying iCCA progression driven by the interplay between platelets and tumor cells, aiming to provide novel therapeutic strategies for iCCA.
methodsThe associations between platelets and cancer development were investigated by analyzing the peripheral blood platelet count, degree of platelet activation and infiltration in the microenvironment of patients with iCCA. By co-culturing tumor cells with platelets, the influence of platelet stimulation on the epithelial-mesenchymal transition (EMT), proliferation, and metastasis of iCCA cells was assessed through in vitro and in vivo experiments. Quantitative proteomic profiling was conducted to identify key downstream targets that were altered in tumor cells following platelet stimulation. The RNA interference technique was utilized to investigate the impacts of gene silencing on the malignant biological behaviors of tumor cells.
resultsCompared with healthy adults, patients with iCCA presented significantly higher levels of peripheral blood platelet counts, platelet activation and infiltration degrees, which were also found to be correlated with patient prognosis. Platelet stimulation greatly facilitated the EMT of iCCA cells, leading to enhanced proliferative and metastatic capabilities. Mechanistically, proteomic profiling identified a total of 67 up-regulated and 40 down-regulated proteins in iCCA cells co-cultured with platelets. Among these proteins, two elevated targets ILK and ITGB3, were further demonstrated to be partially responsible for platelet-induced iCCA progression, which might depend on their regulatory effects on FAK/PI3K/AKT signaling transduction.
conclusionsOur data revealed that platelet-related indices were abnormally ascendant in iCCA patients compared to healthy adults. Co-culturing with platelets enhanced the progression of EMT, and the motility and viability of iCCA cells in vitro and in vivo. Proteomic profiling discovered that platelets promoted the development of iCCA through FAK/PI3K/AKT pathway by means of elevating the expression of ILK and ITGB3, indicating that both proteins are promising therapeutic targets for iCCA with the guidance of platelet-related indices.
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