Cancer is one of the leading causes of death in the world. Despite there are notable improvements in cancer in the past few decades, many cancer patients still cannot be cured due to the development of multi drug resistance (MDR) [1]. Anthraquinones were shown to inhibit tumor growth on various cell lines in previous studies [2,3]. Main anthraquinone aglycons are significant due to their structural similarities to anthracyclines well established anticancer drugs. Therefore aloe-emodin was searched on various cell lines including drug-sensitive CCRF-CEM and multidrug resistant P-glycoprotein-over-expressing CEM/ADR5000 leukemia cells, MDA-MB-231-pcDNA3 breast cancer cells and their transfectant subline MDA-MB-231-BCRP clone 23, HCT116 (p53+/+) colon cancer cells and their knockout clone HCT116 (p53-/-), U87.MG glioblastoma multiform cells and their transfectant subline U87.MGΔEGFR as well as HEK293 human embryonic kidney cells transfected with or without a cDNA for ABCB5. The IC50 values ranged from 21.20µM to 37.32µM for drug-sensitive and wild-type cell lines. For drug-resistant and transfected sublines, IC50 values were ranged from 14.68µM to 66.31µM. Collateral sensitivity (hypersensitivity) to aloe-emodin was observed in HCT116 (p53-/-) knockout cells (0.69 fold). Aloe-emodin having a notable cytotoxicity on few cancer cells needs to be conducted further researches on to clarify the background mechanisms behind its cytotoxicity.
This study was supported by The Scientific and Technological Research Council of Turkey (TÜBITAK) 2214-A scholarship.
[1] Efferth T. Resistance to Targeted ABC Transporters in Cancer. New York: Springer; 2014
[2] Chen YC, Shen SC, Lee WR, Hsu FL, Lin HY, Ko CH, Tseng SW. Biochem Pharmacol 2002; 64: 1713 – 1724
[3] Cichewicz RH, Zhang YJ, Seeram NP, Nair MG. Life Sci 2004; 74: 1791 – 1799
