ArticlePloS one2025
CXCL3 promotes liver cancer progression by modulating the tumor microenvironment via the PI3K/AKT/mTOR pathway.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Caffeine in the Context of Sorafenib Chemotherapy: Insights From Experimental Hepatocarcinogenesis.Journal of biochemical and molecular toxicology · 2026Article
- SOX18 knockdown inhibits colorectal cancer metastasis and angiogenesis through regulation of SAPK/JNK and PI3K/AKT/mTOR signaling pathways.Journal of gastrointestinal oncology · 2026Article
- Unveiling the Intricate Dance: Signaling Pathways in Liver Cancer Metabolism and Immunity.Current oncology reports · 2026Review
- The Interaction of PI3K/AKT/mTOR Pathway with the Tumor Microenvironment: A Dual Engine Driving Breast Cancer Progression and Reshaping Treatment Strategies.Cancer management and research · 2026Review
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Authors and funding
10 authors.
Funding
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Abstract
CXCL3, a member of the CXC chemokine family, has been increasingly implicated in the progression of various cancers, including hepatocellular carcinoma, due to its role in immune and inflammatory responses within the tumor microenvironment. This study aimed to investigate the expression and function of CXCL3 in liver cancer and to elucidate its underlying mechanisms. A combination of bioinformatics analysis, ELISA, RT-qPCR, immunohistochemistry, in vitro cell assays, and in vivo nude mouse models was employed to assess CXCL3 expression and function. The results showed that CXCL3 was significantly upregulated in hepatocellular carcinoma tissues and associated with reduced overall survival in patients. It promoted the proliferation, colony formation, and migration of liver cancer cells (Bel-7402, HepG2, and SMMC-7721) via exogenous, autocrine, and paracrine mechanisms, and recruited tumor-associated macrophages, neutrophils, and fibroblasts into the tumor microenvironment. Mechanistically, CXCL3 activated the PI3K/AKT/mTOR pathway by upregulating PI3K, p-PI3K, AKT, p-AKT, mTOR, and p-mTOR, while the mTOR inhibitor Torin 1 reversed these effects. Gene set enrichment analysis showed enrichment in immune-related pathways, including Toll-like receptor and chemokine signaling. In vivo, CXCL3 overexpression significantly promoted tumor growth in nude mice. These findings suggest CXCL3 facilitates liver cancer progression through tumor microenvironment modulation and PI3K/AKT/mTOR pathway activation.
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