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The development and spread of tumors are significantly influenced by the aberrant activation of oncogenic signaling pathways.
Based on its capacity to target TGF-, PI3K/Akt, MAPK, and NF-B signaling and its influence on invasion and angiogenesis, the current study sought to determine the chemopreventive and therapeutic efficacy of blueberries in the hamster buccal pouch (HBP) carcinogenesis model. 7,12-dimethylbenz[a]anthracene caused squamous cell carcinomas to develop in the HBP (DMBA). Using quantitative real-time PCR and immunoblotting, the impact of blueberries on oncogenic signaling pathways and downstream events was investigated. The ECV304 cell line was used in experiments to investigate how blueberries control angiogenesis. By blocking the TGF- and PI3K/Akt pathways, blueberry supplementation prevented HBP carcinomas from growing and progressing. Although blueberry had no effect on MAPK, it did reduce NF-B activation by preventing NF-B p65 from moving into the nucleus. The expression of the tumor suppressor let-7 and the oncomir miR-21 were both altered by blueberry. Together, these modifications brought to a shift to an anti-invasive and anti-angiogenic phenotype, which was shown by the downregulation of vascular endothelial growth factor and matrix metalloproteinases.
From a therapeutic standpoint, it is crucial to identify the modulatory effects on phosphorylation, intracellular localization of oncogenic transcription factors, and microRNAs as the main mechanisms of action of blueberries. These were all shown by the current study.
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