Studies On Carotenoid And Its Antibreast Cancer Mechanism

To explore the effective mechanism of carotenoid on breast cancer, the breast cancer cell lines MDA-MB-435s (ER-) and MCF-7(ER+) in vitro were used as researching model. The effects of carotenoid on the growth inhibition and apoptosis of breast cancer cell lines were detected by MTT assay, acridine orange/ethidium bromide double fluorescent dye staining method and TUNEL assay; The proliferation cycle, DNA damage and gene expression of breast cancer cell were also studied. The main results are as follows:1. The effects of carotenoid on the growth inhibition of human breast cancer cell lines.The restrain of carotenoid to the growth of human breast cancer cell lines MDA-MB-435S and MCF-7 was detected by MTT assay. The results showed that different types of carotenoid have different effects on the growth of the breast cancer cell lines B -carotene and astaxanthin could inhibit the growth of human breast cancer cell lines MDA-MB-435S and MCF-7 effectly. The effects of carotenoid on the growth inhibition of breast cancer cell lines were enhanced with the enhancing of concentration and time of carotrnoids and showed obviously dose-response and time-response relationship. Zeaxanthin and Zeaxanthin dipahviitate could promote the growth of human breast cancer cell lines MDA-MB-435s but have little effect to the growth of human breast cancer cell lines MCF-7. Canthaxanthin could promote the growth of MDA-MB-435S and restrain the growth of human breast cancer cell lines MCF-7. Lycopene could restrain the growth of human breast cancer cell lines MDA-MB-435S, but has little effect to the growth of human breast cancer cell lines MCF-7.2. The effect of carotenoid on the human breast cancer cell apoptosis The human breast cancer cell apoptosis were detected by the acridine orange/ethidium bromide double fluorescent dye staining method and TUNEL assay. The apoptosis positive cells could be observed in the breast cancer cell lines MDA-MB-435s treated by B -carotene, astaxanthin and lycopene, but there were not apoptosis positive cells in the breast cancer cell lines MDA-MB-435s treated by canthaxanthin zeaxanthin and zeaxanthin dipalmitate; Theapoptosic positive cells could be observed in the breast cancer cell lines MCF-7 treated by B -carotene, astaxanthin and canthaxanthin,but there were not apoptosis positive cells in the breast cancer cell lines MDA-MB-435s treated by lycopene. zeaxanthin and zeaxanthin dipalmitate, These results suggest that B -carotene, astaxanthin and lycopene could increase the apoptosis of breast cancer cell lines MDA-MB-435S cell, but canthaxanthin zeaxanthin and zeaxanthin dipalmitate have little effect on it. B -carotene, astaxanthin and canthaxanthin could increase the apoptosis of breast cancer cell lines MCF-7 cell, but lycopene zeaxanthin and zeaxanthin dipalmitate have little effect on it.3. The effect of carotenoid on the DNA damage of breast cancer cell The DNA damage of breast cancer cell was determined by the single cell gel electrophoresis assay. B -carotene and astaxanthin could induce the DNA damage of breast cancer cell lines MDA-MB-435s and MCF-7 and show dose-response and time-response relationship. Zeaxanthin and zeaxanthin dipalmitate could not induce the DNA damage of breast cancer cell lines MDA-MB-435s and MCF-7. Canthaxanthin could induce the DNA damage of breast cancer cell lines MCF-7 but could not induce the DNA damage of breast cancer cell lines MDA-MB-435S. Lycopene could induce the DNA damage of breast cancer cell lines MDA-MB-435s but could not induce the DNA damage of breast cancer cell lines MCF-74. The effect of carotenoid on the proliferation cycle of breast cancer cellThe effect of carotenoid to proliferation cycle of breast cancer cell was detected by flow cytometer assay. The result showed that carotenoid have no effect on the proliferation cycle of breast cancer cell lines MDA-MB-435s and MCF-7.5. The effect of carotenoid on the gap junctional communication of breast cancer cell The effect of carotenoid on the gap junctional communicati...