Fig. 4

Cantharisin exhibits therapeutic potential against pancreatic and lung cancers by modulating RAD51 and BRCA1 in HRR pathway. By inhibiting the Nrf2 pathway, Cantharisin decreases the expression of RAD51, thereby increasing DNA damage in cancer cells. Additionally, it modulates the expression of RAD51 and BRCA1 via the activation of the p53 signaling pathway, which enhances DNA repair mechanisms and cell cycle checkpoints. It downregulates the expression of RAD51, thereby reducing the capacity of cancer cells to repair DNA by inhibiting the PI3K/Akt and ERK/MAPK signaling pathways. Additionally, it indirectly upregulates BRCA1 expression, thereby enhancing DNA repair mechanisms through the inhibition of the PI3K/Akt and NF-κB pathways. This compound contributes to the heightened reliance of cancer cells on DNA damage response by augmenting oxidative stress, which subsequently impairs the repair functions of RAD51 and BRCA1, leading to increased cellular apoptosis