Antitumor Effects of Miconazole on Human Colon Carcinoma Xenografts in Nude Mice through Induction of Apoptosis and G0/G1 Cell Cycle Arrest

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

“…The cytotoxic effects of MIC in both bladder cancer cell lines were similar to that previously reported for colon cancer cells (COLO205; IC 50 ~50 µM) (12). MIC caused cell cycle arrest at G0/G1 transition in both the T24 and TSGH-8301 cells.…”

“…MIC has also been shown to be an effective anticancer drug. For example, MIC was found to inhibit the proliferation of human acute myelogenous leukemia (10) and breast and bladder cancer cells (11), and to induce apoptosis through G0/G1 cell cycle arrest in some types of human colorectal cancer cell lines (12). Other studies have revealed that MIC may inhibit melanogenesis in B16 cells and that MIC may be useful in the treatment of hyperpigmentation disorders, such as ephelis and melasma (13).…”

Study of the Anti-Proliferative Activity of 5-Substituted 4,7-Dimethoxy-1,3-Benzodioxole Derivatives of SY-1 fromAntrodia camphorataon Human COLO 205 Colon Cancer Cells

“…As shown in Figure 2(a), significant G0/G1 arrest was induced in COLO 205 cells treated with apiole (>75  μ M), and this effect was dose dependent. Our previous study showed that cyclin-dependent kinase inhibitors (CDKi), such as p21 and p27, are upregulated in human colon cancer cells arrested in G0/G1 by treatment with anti-cancer agents [4, 15, 16]. In the present study, COLO 205 cells exposed to apiole (<150  μ M) displayed induction of p21, p27 and p53 and decreased expression of cyclin D1 (Figure 2(b)).…”

A survey on anticancer effects of artemisinin, iron, miconazole, and butyric acid on 5637 (bladder cancer) and 4T1 (Breast cancer) cell lines

“…They used deoxyribonucleic acid (DNA) fragmentation and the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and concluded that miconazole treatment caused apoptosis in human colon carcinoma tumor tissues. [9] In our study the dominance of pathological changes deviated from apoptosis to necrosis following miconazole administration. The presence or absence of miconazole or butyric acid in different groups clarified the role of these two agents and showed that miconazole played the main role in causing necrosis and of course biochemical changes.…”

“…This growth arrest was dose-dependent and probably related to the p53 signaling pathway. [9] Transitional cell carcinoma is classified among the most lethal cancers in the United States. This neoplastic disease is highly invasive because of its metastasis and recurrence.…”