Modulation of Multidrug Resistance and Apoptosis of Cancer Cells by Selected Carotenoids

• Published in: In vivo (Athens) Vol. 18; no. 2; pp. 237 - 244
• Main Authors: Molnár, Joseph, Gyémánt, Nóra, Mucsi, Ilona, Molnár, Annamária, Szabó, Margaret, Körtvélyesi, Tamás, Varga, András, Molnár, Péter, Tóth, Gyula
• Format: Journal Article
• Language: English
• Published: Greece International Institute of Anticancer Research 01-03-2004
• Subjects: Animals; Apoptosis - drug effects; Capsicum - chemistry; Carotenoids - chemistry; Carotenoids - pharmacology; Cell Line, Tumor; Drug Resistance, Multiple - drug effects; Drug Resistance, Multiple - genetics; Genes, MDR; Humans; Mice; Neoplasms - drug therapy; Neoplasms - genetics; Neoplasms - metabolism; Plant Extracts - chemistry; Plant Extracts - pharmacology; Rhodamine 123 - metabolism; Transfection
• ISSN: 0258-851X; 1791-7549

The multidrug resistance (MDR) proteins that belong to the ATP-binding casette superfamily are present in a majority of human
tumors and are an important final cause of therapeutic failure. Therefore, compounds which inhibit the function of the MDR-efflux
proteins may improve the cytotoxic action of anticancer chemotherapy. The effects of carotenoids were studied on the activity
of the MDR-1 gene-encoded efflux pump system. The carotenoids, isolated from paprika and other vegetables, were tested on
the rhodamine 123 accumulation of human MDR-1 gene-transfected L1210 mouse lymphoma cells and human breast cancer cells MDA-MB-231
(HTB-26). Capsanthin and capsorubin enhanced the rhodamine 123 accumulation 30-fold relative to nontreated lymphoma cells.
Lycopene, lutein, antheraxanthin and violaxanthin had moderate effects, while alfa- and beta-carotene had no effect on the
reversal of MDR in the tumor cells. Apoptosis was induced in human MDR1 transfected mouse lymphoma cells and human breast
cancer MDA-MB-231 (HTB-26) cell lines in the presence of lycopene, zeaxanthin and capsanthin. The data suggest the potential
of carotenoids as possible resistance modifiers in cancer chemotherapy.