Gallic Acid Targets a New Prostate Cancer Progression Pathway

A new preclinical study has identified the NF-κB/KLF7/L1CAM axis as a potential driver of prostate cancer progression and shown that gallic acid can interfere with this pathway. KLF7 was found to promote proliferation, migration and invasion by activating L1CAM, a protein associated with aggressive and metastatic behaviour. Upstream, phosphorylation of the NF-κB p65 subunit appeared to act as a key regulator of the pathway.
Gallic acid, a naturally occurring polyphenol found in several plants and foods, bound to NF-κB p65 and inhibited its phosphorylation, reducing KLF7 and L1CAM activity. In PC-3 and LNCaP prostate cancer cells, this suppressed proliferation, invasion and migration, while the researchers reported no comparable toxicity in normal prostate stromal cells.
The effect was also tested in mice, where oral gallic acid reduced tumour volume and weight. According to the study report, its antitumour activity was comparable to enzalutamide or bicalutamide in the experimental model, while combinations produced stronger effects.
The findings are intriguing because they point not only to gallic acid itself but to a potentially druggable NF-κB → KLF7 → L1CAM pathway involved in aggressive prostate cancer behaviour. However, the evidence remains entirely preclinical: no prostate cancer patients were treated, and the doses and exposures achievable in humans may differ substantially from those used experimentally.
For now, gallic acid should therefore be viewed as a research lead rather than a treatment, but the newly identified pathway may provide a useful target for future therapies aimed at invasion and metastatic progression.

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