Abstract
Abstract Salinomycin isolated from Streptomyces albus and a potassium ionophore. It has been used to eliminate bacteria, fungi and parasites. Also, Cancer stem cells (CSCs) are a subpopulation of cells within the tumor that has ability to self-renew and undergo differentiation to phenotypically diverse cell populations. So, CSCs are involved in metastasis, chemoresistance and even cancer relapse. Recently, there are many evidences to CSCs subpopulations enhance capability of DNA repair and reduce the apoptosis. Furthermore, salinomycin has been reported to act as selective breast cancer stem cell inhibitor based on its property of reducing the cancer stem cell and to induce the apoptosis in cancer cell. Therefore, we investigated the effect of salinomycin on breast cancer stem cells. First, Mammosphere formation assay was performed to observe stem cell-like property after salinomycin treat in anchorage-independent state. We confirmed salinomycin reduces number and size of mammosphere at 3, 6, 9 day. Also, we compared mRNA expressing level of stem cell marker such as SOX2 and OCT4 by RT-PCR. Consequently, salinomycin was the down-regulated stem cell marker mRNA level as well as protein level. To confirm the reduction of the side population level, we performed FACS analysis using CD44+ and CD24- markers. Results by FACS analysis revealed that salinomycin treated with breast cancer stem cell reduced stemness by downregulating CD44+/CD24- population. Consistently, when mammosphere implanted into the mammary fat pads of BALB/c female nude mice cleared of endogenous epithelium, the tumor size was decreased. In conclusion, we concluded that effect of salinomycin to reduce stemness is mediated by downregulation of SOX2 and OCT4 in human breast cancer cell. Citation Format: Hyun Sook An, Han Na Kang, Myoung Hee Kang, Jung Lim Kim, Jun Suk Kim, Jae Hong Seo. Salinomycin reduced breast cancer stem cell properties by reducing SOX2 and OCT4. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3724. doi:10.1158/1538-7445.AM2013-3724
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