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  • Title: [Effects and its mechanism of quercetin on cervical cancer HeLa cells].
    Author: Huang LQ, Zhang W, Yang Y, Tao L.
    Journal: Zhonghua Fu Chan Ke Za Zhi; 2009 Jun; 44(6):436-9. PubMed ID: 19953944.
    Abstract:
    OBJECTIVE: To evaluate the effects of quercetin on HeLa cells proliferation and study the mechanism of apoptosis. METHODS: The proliferation of HeLa cells treated with quercetin at different concentrations (6.25, 12.5, 25, 50 micromol/L) for 24 hours was assessed by methyl thiazolyl tetrazolium (MTT) method, and also observe the inhibitory effect of quercetin on the transplanted carcinoma in BALB/ C nude mice. Cell apoptosis rate was detected by flow cytometry with annexin V- fluorescein isothiocyannate (FITC)/propidium iodide (PI) technology. The changes of intracellular calcium ion concentration ([Ca2+]i) and mitochondrial membrane potential in HeLa cells induced by quercetin were studied by laser confocal fluorescence microscope and specificity fluorescent probes of Fluo-3/AM and JC-1. Colorimetric method was used to measure the activity of caspase-3. RESULTS: After treated by different concentrations of quercetin (6.25, 12.5, 25, 50 micromol/L), the proliferation was inhibited and the apoptosis was induced in HeLa cells with the inhibition rate of (13.4 +/- 2.2)%, (26.2 +/- 6.8)%, (39.8 +/- 11.4)% and (48.5 +/- 9.1)% respectively, and with the apoptosis rate of (9.0 +/- 1.4)%, (13.3 +/- 1.1)%, (22.5 +/- 2.3)% and (44.7 +/- 4.2)% respectively, and which effects were dose-dependent (P < 0.01). Treated by different concentrations of quercetin (25, 50, 100 mg kg(-1) d(-1)), the growth of transplanted tumor in nude mice was inhibited with the inhibition rate of 13.4%, 30.4%, 45.8%. The apoptosis of HeLa cells was induced by quercetin, which markedly reduced mitochondrial membrance potential, effectively enhance [Ca2+]i, and the caspase-3 was activated in a dose-dependent manner (P < 0.01). CONCLUSION: Quercetin can significantly inhibit the proliferation of HeLa cells, which may be induced apoptosis of cervical cancer cells via the Ca2+ -dependent mitochondrial apoptosis pathway.
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