Effect of dexamethasone on extracellular secretion of cystatin C in cancer cell lines
- Authors:
- Chika Yamawaki
- Minoru Takahashi
- Kohji Takara
- Manabu Kume
- Midori Hirai
- Hiroyuki Yasui
- Tsutomu Nakamura
View Affiliations
Affiliations: Department of Pharmaceutical Health Care, Faculty of Pharmaceutical Sciences, Himeji Dokkyo University, Himeji, Hyogo 670-8524, Japan, Department of Pharmacy, Kobe University Hospital, Kobe, Hyogo 650-0017, Japan, Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University, Kyoto 607-8414, Japan
- Published online on: October 12, 2012 https://doi.org/10.3892/br.2012.21
-
Pages:
111-114
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Abstract
The aim of the present study was to investigate dexamethasone (DEX)-induced secretion of cystatin C (Cys C) and the effect of cisplatin (CDDP) and 5-fluorouracil (5‑FU) on Cys C secretion in human cancer cell lines. KYSE150, A549 and Caki‑2 human cancer cell lines were cultured on plastic dishes and treated with DEX (100 nM) for 24, 48 and 72 h. KYSE150 cells were co‑treated with DEX, CDDP (10 µM), and 5‑FU (2 µM). The effects of DEX, CDDP and 5‑FU on cell viability were evaluated. Results showed Cys C secretion levels in the culture medium of DEX-treated KYSE150 cells to be 1.8- to 2.3‑fold higher compared to those in the culture medium of control cells. A similar tendency was observed in A549 cells at all the time points, whereas a significant increase in the Cys C secretion by Caki‑2 cells was observed only 24 h after DEX treatment. Regarding KYSE150 cells, the secretion of Cys C was also enhanced by co‑treatment of CDDP or 5‑FU with DEX, although it was not affected by the co‑administration of DEX and mifepristone, a glucocorticoid receptor antagonist. At concentrations that are typically used in esophageal cancer chemotherapy, CDDP and 5‑FU demonstrated a moderate level of cytotoxicity in KYSE150 cells in contrast to DEX. These findings suggested that DEX has the potential to enhance the extracellular secretion of Cys C in esophageal cancer cells, possibly due to the transcriptional regulation mediated by glucocorticoid receptor activity.
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