Leonurine suppresses prostate cancer growth in vitro and in vivo by regulating miR-18a-5p/SLC40A1 axis.

Prostate cancer is a leading cause of cancer-associated death in males. Leonurine (Leo) is a pleiotropic anti-tumor agent isolated from traditional Chinese herb that was used in gynecologic treatments. However, its pharmacological effect against prostate cancer progression remains unclear. Here, we showed that Leo dose dependently inhibited prostate cancer cell proliferation, promoted cell apoptosis, and induced cell cycle arrest. Moreover, we noticed that miR-18a-5p was downregulated and the solute carrier family 40 member 1 (SLC40A1) is upregulated by Leo treatment. SLC40A1 knockdown by siRNA abrogated the inhibitory effect of Leo on prostate cancer progression. Notably, Leo also significantly inhibited prostate cancer progression in a subcutaneous xenograft tumor mouse model in vivo. This study further unveiled the mechanism by which Leo inhibited prostate cancer progression, which provides a promising potential for its future clinical application.

Upregulation of miR-18a-5p promotes the proliferation of prostate cancer via inhibiting the expression of SLC40A1.

Prostate cancer (PCa) is the most commonly diagnosed cancer in males and the fifth most common cause of cancer death worldwide. Previous studies indicated that miR-18a-5p modulated epithelial-mesenchymal transition in breast cancer via targeting SREBP1 forming a co-repressor complex with Snail and HDAC1/2. However, the function of miR-18a-5p in prostate cancer remains largely unknown. In this study, we identified miR-18a-5p as a tumor promoter in prostate cancer. miR-18a-5p expression was found upregulated in human prostate cancer tissues while SLC40A1 was down-regulated. Cell proliferation assay demonstrated that miR-18a-5p promoted prostate cancer cell proliferation. We also found SLC40A1 was downregulated by miR-18a-5p in prostate cancer cell lines. Restoration of SLC40A1 reversed the effects of miR-18a-5p in prostate cancer cells. Taken together, our results suggest that miR-18a-5p might function as a tumor-promoting factor in PCa and might contribute to its proliferation.