ArticleHereditas2025
CAFs-derived SPI1 in tumor fibroblasts promotes malignant behaviors of liver cancer cells and immune escape by regulating HRAS and PD-L1 transcription.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Metabolic reprogramming-driven resistance to multi-kinase inhibitors in hepatocellular carcinoma: molecular mechanisms and therapeutic opportunities.Molecular cancer · 2026Review
- Tryptophan metabolism in tumor immune escape: mechanisms, cellular crosstalk, and therapeutic opportunities.Frontiers in immunology · 2026Review
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Authors and funding
3 authors.
Funding
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Abstract
backgroundAs the fifth most common cancer worldwide, hepatocellular carcinoma (HCC) is a highly malignant disease with a formidable prognosis. Within the tumor microenvironment, cancer-associated fibroblasts (CAFs) play a paramount role in tumorigenesis and progression by providing a supportive environment for cancer cells. This research aims to elucidate the regulatory mechanisms of CAFs and salmonella pathogenicity island 1 (SPI1) in HCC progression.
methodsProtein and mRNA expression levels were determined by western blot and reverse-transcription quantitative polymerase chain reaction (RT-qPCR), respectively. The ability of glycolysis was detected using the glucose consumption and lactate production test kit. Cell proliferation was examined using colony formation assay. Cell migration and invasion were assessed via wound healing and transwell assays, respectively. The cell apoptosis was examined by flow cytometry and terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL).
resultsThe CAFs and para-cancer fibroblasts (PAFs) were successfully separated. CAFs under hypoxic stress (H/CAFs) promoted glucose consumption and lactate production in HCC cells (Huh7 and Hep3B). CAFs conditioned medium (CAFs-CM) facilitated HCC cell proliferation, migration, invasion, glucose consumption, and lactate production. CAFs-CM facilitated programmed cell death 1 ligand 1 (PD-L1) and CD8
conclusionsSPI1 derived from CAFs facilitates the malignant behaviors of HCC cells by up-regulating v-Ha-ras Harvey rat sarcoma viral oncogene homolog (HRAS) expression. This study enriches our understanding of HCC at the molecular level and may pave the way for the development of a novel strategy for the treatment of HCC.
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