Sulforaphane suppresses the viability and metastasis, and promotes the apoptosis of bladder cancer cells by inhibiting the expression of FAT‑1
- Fei Wang
- Penghua Liu
- Hexiang An
- Yu Zhang
Affiliations: Shenzhen Key Laboratory of Viral Oncology, Clinical Innovation and Research Center, Shenzhen Hospital of Southern Medical University, Shenzhen, Guangdong 518101, P.R. China, Department of Urology, Baoan Central Hospital of Shenzhen, The Fifth Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong 518102, P.R. China
- Published online on: July 2, 2020 https://doi.org/10.3892/ijmm.2020.4665
Copyright: © Wang
et al. This is an open access article distributed under the
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FAT atypical cadherin 1 (FAT1) regulates complex mechanisms for the promotion of oncogenesis or the suppression of malignancies. Sulforaphane (SFN) has antioxidant and anti‑tumor activities. The present study investigated the roles of SFN and FAT1 in bladder cancer (BC). The expression of FAT1 in BC cell lines and tissues was measured by western blot analysis and reverse transcription‑quantitative PCR (RT‑qPCR). The association between FAT1 expression and the 5‑year survival rate of patients with BC was evaluated. The viability of and FAT1 expression in T24 and SW780 cells exposed to various concentrations of SFN were detected by MTT assay, and western blot analysis and RT‑qPCR, respectively. Furthermore, the viability, migration, invasion and apoptosis of and FAT1 expression in BC cells subjected to FAT1 overexpression or knockdown, and with or without SFN stimulation, were examined. The results revealed that FAT1 expression in BC cells and tissues was increased, and patients with a high FAT‑1 expression had a shorter 5‑year survival time than those with a low FAT‑1 expression. BC cell viability and FAT1 expression were suppressed by SFN in a concentration‑dependent manner. The knockdown of FAT1 inhibited the viability, migration and invasion, and promoted the apoptosis of BC cells, whereas the overexpression of FAT1 produced opposite effects. In addition, cells exposed to SFN exhibited a reduced viability, migration, invasion and an increased apoptosis, effects which were promoted by FAT1 knockdown; however, the overexpression of FAT1 blocked the above‑mentioned effects of SFN on the cells. On the whole, the present study demonstrates that SFN suppresses the progression of BC by inhibiting the expression of FAT‑1; thus, SFN may be used as a potential drug for the treatment of BC.