Abstract
The anti-cancer properties of curcumin in vitro have been documented. However, its clinical use is limited due to rapid metabolization. Since irradiation of curcumin has been found to increase its anti-cancer effect on several tumor types, this investigation was designed to determine whether irradiation with visible light may enhance the anti-tumor effects of low-dosed curcumin on renal cell carcinoma (RCC) cell growth and proliferation. A498, Caki1, and KTCTL-26 cells were incubated with curcumin (0.1–0.4 µg/mL) and irradiated with 1.65 J/cm2 visible light for 5 min. Controls were exposed to curcumin or light alone or remained untreated. Curcumin plus light, but not curcumin or light exposure alone altered growth, proliferation, and apoptosis of all three RCC tumor cell lines. Cells were arrested in the G0/G1 phase of the cell cycle. Phosphorylated (p) CDK1 and pCDK2, along with their counter-receptors Cyclin B and A decreased, whereas p27 increased. Akt-mTOR-signaling was suppressed, the pro-apoptotic protein Bcl-2 became elevated, and the anti-apoptotic protein Bax diminished. H3 acetylation was elevated when cells were treated with curcumin plus light, pointing to an epigenetic mechanism. The present findings substantiate the potential of combining low curcumin concentrations and light as a new therapeutic concept to increase the efficacy of curcumin in RCC.
Highlights
Cancer is the second most common cause of death in Europe
When visible light was applied, DNA fragments significantly increased in all three cell lines, even at 0.1 μg/mL curcumin
As low as 0.1 μg/mL (Caki1 and KTCTL-26) or 0.2 μg/mL curcumin (A498) significantly reduced tumor cell growth following irradiation, while 0.1 or 0.2 μg/mL curcumin alone or with light alone did not lead to growth-blocking effects in any of these cell lines
Summary
The incidence of renal cell carcinoma (RCC) is, compared to other cancer types, relatively rare, but both incidence and mortality are steadily increasing at a rate of approximately 2% to 3% per decade. Approximately 3% of all adult cancer patients suffer from malignant kidney tumors [1,2]. RCC is the most frequent form of kidney neoplasm, comprising about 90–95% of all renal melanomas [3]. One third of these patients have metastases at diagnosis, and 30–70% of patients with localized disease relapse within 5 years of surgery [4]. Since metastatic RCC (mRCC) is resistant to most treatments such as conventional chemotherapy or radiation, patients with mRCC can expect a 5 year survival rate of less than 10% [5]. The introduction of targeted agents including the tyrosine kinase inhibitors, sunitinib and sorafenib, and the mechanistic target of rapamycin (mTOR) inhibitors, temsirolimus and everolimus, have substantially improved patient outcome, but these drugs are not curative due to inevitable resistance development during therapy
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