Miconazole induces apoptosis via the death receptor 5-dependent and mitochondrial-mediated pathways in human bladder cancer cells

Oncology Reports
Sheau-Yun YuanKan-Jen Tsai

Abstract

Miconazole (MIC), an antifungal agent, diplays anti‑tumorigenic activity in various types of human cancers, including bladder cancer, yet its mechanism of antitumor action is not well understood. In the present study, we demonstrated that, in a cell viability assay, MIC had a cytotoxic effect on human T24, J82 and TSGH-8301 bladder cancer cells in a dose- and time‑dependent manner, but did not exhibit significant toxicity toward human peripheral blood mononuclear cells. Cell cycle analysis revealed that MIC at concentrations of 25 and 50 µM significantly caused G0/G1 arrest in the TSGH-8301 and T24 cells, respectively. DNA fragmentation, mitochondrial membrane potential and western blot analyses showed that MIC inhibited the growth of these cells by both mitochondrial‑mediated and death receptor (DR5)‑mediated apoptosis pathways. Specifically, MIC increased the protein levels of p21 and p27, but decreased the expression of cyclin E1, CDK2 and CDK4. MIC augmented the expression of DR5, cleaved forms of caspase-3 -8 and -9, poly(ADP‑ribose) polymerase and Bax, decreased the expression of Bcl-2 but increased cytosol levels of cytochrome c. Our results suggest that MIC inhibits the growth of bladder cancer cells through induction o...Continue Reading

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Citations

Feb 6, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Tomhiro MastuoHideki Sakai
Sep 28, 2020·Environmental Toxicology·Chao-Yen HoThomas I-Sheng Hwang
Apr 27, 2019·Frontiers in Oncology·Julieti Huch BussFabiana Kömmling Seixas
Oct 6, 2018·European Journal of Pharmacology·Chen-Li ChengSheau-Yun Yuan
Jul 3, 2021·Journal of Fungi·Anne Caroline Morais CaldeirãoDouglas Roberto Monteiro

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