Abstract
Bladder cancer (BC) is a common form of urinary tract tumor, and its incidence is increasing annually. Unfortunately, an increasing number of newly diagnosed BC patients are found to have advanced or metastatic BC. Although current treatment options for BC are diverse and standardized, it is still challenging to achieve ideal curative results. However, Sulforaphane, an isothiocyanate present in cruciferous plants, has emerged as a promising anticancer agent that has shown significant efficacy against various cancers, including bladder cancer. Recent studies have demonstrated that Sulforaphane not only induces apoptosis and cell cycle arrest in BC cells, but also inhibits the growth, invasion, and metastasis of BC cells. Additionally, it can inhibit BC gluconeogenesis and demonstrate definite effects when combined with chemotherapeutic drugs/carcinogens. Sulforaphane has also been found to exert anticancer activity and inhibit bladder cancer stem cells by mediating multiple pathways in BC, including phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), mitogen-activated protein kinase (MAPK), nuclear factor kappa-B (NF-κB), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), zonula occludens-1 (ZO-1)/beta-catenin (β-Catenin), miR-124/cytokines interleukin-6 receptor (IL-6R)/transcription 3 (STAT3). This article provides a comprehensive review of the current evidence and molecular mechanisms of Sulforaphane against BC. Furthermore, we explore the effects of Sulforaphane on potential risk factors for BC, such as bladder outlet obstruction, and investigate the possible targets of Sulforaphane against BC using network pharmacological analysis. This review is expected to provide a new theoretical basis for future research and the development of new drugs to treat BC.