ArticleMolecular and cellular biochemistry2026
Cancer-associated fibroblasts-secreted exosomes promote malignant advancement of liver cancer by regulating the circE2F3/miR-1305/E2F3 axis.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Liver cancer is a highly lethal malignancy. Cancer-associated fibroblasts (CAFs) play a key role in regulating tumor progression, in part through the release of exosomes. This study aimed to investigate whether CAF-derived exosomes contribute to the progression of liver cancer. CAFs were isolated from human liver tumor tissues, and exosomes were subsequently purified from the CAF-conditioned medium. Cell viability was measured using the Cell Counting Kit-8 assay. Cell migration was evaluated by Transwell and wound healing assays. The expression levels of circE2F3, miR-1305, and E2F3 were quantified by quantitative real-time PCR. The interactions among them were validated via luciferase reporter assays and RNA pull-down experiments. CAFs promoted the viability and migration of liver cancer cells. Exosomes derived from CAFs similarly enhanced the proliferative and migratory capacities of these cells. Upon exosomal treatment, circE2F3 expression was upregulated in liver cancer cells. Mechanistically, circE2F3 functioned as a molecular sponge for miR-1305, which directly targets E2F3. Knockdown of circE2F3 suppressed the malignant behaviors of liver cancer cells by modulating the miR-1305/E2F3 axis. Furthermore, inhibiting circE2F3 counteracted the tumor-promoting effects of CAF-derived exosomes, concomitant with altered expression of miR-1305 and E2F3. CAF-derived exosomes promote liver cancer progression by upregulating circE2F3, which in turn sequesters miR-1305 and elevates E2F3 expression. These findings highlight CAF-derived exosomal circE2F3 as a potential therapeutic target for liver cancer.
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