20 Prostate cancer is the second most common malignancy in men worldwide, with incidence ranking highly among male cancers in many countries. Androgen deprivation therapy remains the primary treatment, but many patients inevitably progress to castration resistant prostate cancer, in which tumours continue to grow despite treatments that lower androgen levels. Standard options include androgen receptor inhibitors such as enzalutamide and bicalutamide. The complex molecular mechanisms underlying this progression highlight the need to identify new, effective, and safe therapeutic targets. A research team led by Professor Jun Zhang from Shihezi University School of Medicine in China focused on the transcription factor Krüppel Like Factor 7 (KLF7). Their findings were made available online on 15th July 2026 in the Chinese Medical Journal. Using RNA sequencing to identify gene expression patterns and bioinformatics analysis to map relationships, the team found that KLF7 is highly expressed in prostate cancer and acts as a direct transcriptional activator of L1 Cell Adhesion Molecule (L1CAM), a key protein associated with tumour metastasis. KLF7 overexpression drives L1CAM production and supports metastatic behaviour in prostate cancer cells. The study also found that phosphorylation of the NF κB p65 subunit acts as the master regulator of this axis, while blocking that phosphorylation interrupts the signalling cascade. Gallic acid is a naturally occurring phenolic compound found in various plants, including tea leaves, grapes, and other fruits. Previous laboratory studies have examined its effects on prostate cancer cells through mechanisms such as influencing cell cycle progression and migration. The current work builds on these findings by identifying a specific molecular pathway involving NF κB, KLF7, and L1CAM that gallic acid can interrupt. Using surface plasmon resonance and molecular docking, biophysical methods that confirmed the direct interaction, the researchers showed that gallic acid forms a stable complex with NF κB p65, specifically targeting the serine 276 phosphorylation site. By inhibiting this phosphorylation, gallic acid blocks the downstream KLF7/L1CAM pathway. In vitro experiments showed that gallic acid significantly impaired aggressive behaviours in PC 3 and LNCaP cells, limiting proliferation, invasion, and migration in both androgen sensitive LNCaP cells and the more aggressive PC 3 line. It did so without exhibiting toxicity to normal prostate stromal cells. In vivo, the team used a high fat diet induced obesity mouse model because obesity is associated with more aggressive prostate cancer features in some patients. Oral administration of gallic acid significantly reduced tumour volume and weight without noted harm to surrounding normal tissue. The anti tumour efficacy of gallic acid was comparable to conventional drugs such as enzalutamide and bicalutamide, while combination therapy showed enhanced therapeutic outcomes. The study provides a theoretical basis for further investigation of gallic acid as a potential treatment for advanced prostate cancer. The findings suggest it could offer an additional approach, either alone or alongside standard agents, particularly given its apparent lack of toxicity to healthy prostate cells in laboratory tests. However, further clinical studies are needed to assess its safety, dosing, and efficacy in humans. Identifying the NF κB/KLF7/L1CAM axis as a potential therapeutic target may also guide the development of related agents. The work from the Shihezi University team provides further mechanistic insight into how gallic acid affects prostate cancer cells and highlights a pathway that could be explored in future research.