Purpose: CC-chemokine ligand 11 (CCL11; eotaxin-1), an eosinophil chemoattractant chemokine, has been proposed as a serum marker for prostate cancer (PCa) by two research groups. We investigated the usefulness of CCL11 in diagnosing prostatic diseases, such as benign prostatic hyperplasia (BPH) and PCa. Materials and Methods: CCL11 was measured in the sera of 139 men with BPH, 44 men with PCa, and 45 control men attending an outpatient health-screening clinic. A commercial enzyme-linked immunosorbent assay kit was used to measure CCL11. Results: CCL11 concentrations were significantly higher in men with BPH and PCa than in normal men (72.9±3.15 and 80.0±4.91 pg/ml vs. 57.6±8.24). In addition, a receiver operating characteristic (ROC) analysis of serum CCL11 levels showed that the areas under the ROC curves were 0.661 (p=0.001) and 0.654 (p=0.012) for BPH and PCa, respectively, compared with normal men. Conclusions: CCL11 may be helpful in diagnosing prostatic diseases, such as BPH and PCa.
Renal cell carcinoma (RCC) frequently recurs or metastasizes after surgical resection. Everolimus, an mTOR inhibitor, is used as a second-line treatment, but the response of RCC to everolimus is insufficient. Metformin is an antidiabetic drug; recent reports have indicated its anti-cancer effects in various cancers, and it is known to have synergistic effects with other drugs. We investigated the possibility of coadministering everolimus and metformin as an effective treatment for RCC. RCC cells treated with a combination of the two drugs showed significantly inhibited cell viability, cell migration, and invasion, and increased apoptosis compared to those treated with each drug alone. An anti-cancer synergistic effect was also confirmed in the xenograft model. Transcriptome analysis for identifying the underlying mechanism of the combined treatment showed the downregulation of mitochondrial fusion genes and upregulation of mitochondrial fission genes by the combination treatment. Changes in mitochondrial dynamics following the combination treatment were observed using LysoTracker, LysoSensor, and JC-1 staining. In conclusion, the combination of everolimus and metformin inhibited RCC growth by disrupting mitochondrial dynamics. Therefore, we suggest that a treatment combining metformin and everolimus disrupts mitochondrial dynamics in RCC, and may be a novel strategy for RCC treatment.
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