期刊
INTERNATIONAL JOURNAL OF NANOMEDICINE
卷 10, 期 -, 页码 5505-5512出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/IJN.S83838
关键词
realgar; quantum dots; apoptosis; necrosis; endoplasmic reticulum stress; endometrial cancer cells
资金
- Science and Technology Foundation of Guizhou [CK-856, 2013-03]
- Key Lab Construction Project of the Educational Department of Guizhou [KY[2014]212]
- Harbin Institute of Technology (HIT) [AUGA4110005410]
- Fundamental Research Funds for the Central Universities [HIT. IBRSEM. 201331]
- Program for Innovation Research of Science in Harbin Institute of Technology (PIRS of HIT) [201411]
Realgar (A(S4)S(4)) has been used in traditional medicines for malignancy, but the poor water solubility is still a major hindrance to its clinical use. Realgar quantum dots (RQDs) were therefore synthesized with improved water solubility and bioavailability. Human endometrial cancer JEC cells were exposed to various concentrations of RQDs to evaluate their anticancer effects and to explore mechanisms by the MTT assay, transmission electron microscopy (TEM), flow cytometry, real-time reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot analysis. Results revealed that the highest photoluminescence quantum yield of the prepared RQDs was up to approximately 70%, with the average size of 5.48 nm. RQDs induced antiproliferative activity against JEC cells in a concentration-dependent manner. In light microscopy and TEM examinations, RQDs induced vacuolization and endoplasmic reticulum (ER) dilation in JEC cells in a concentration-dependent manner. ER stress by RQDs were further confirmed by increased expression of GADD153 and GRP78 at both mRNA and protein levels. ER stress further led to JEC cell apoptosis and necrosis, as evidenced by flow cytometry and mitochondrial membrane potential detection. Our findings demonstrated that the newly synthesized RQDs were effective against human endometrial cancer cells. The underlying mechanism appears to be, at least partly, due to ER stress leading to apoptotic cell death and necrosis.
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