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. 2019 Mar;17(3):1523-1528.
doi: 10.3892/etm.2018.7104. Epub 2018 Dec 17.

Allicin suppresses the migration and invasion in cervical cancer cells mainly by inhibiting NRF2

Qiumei Zhang  1 , Dongmei Yang  1   2
Affiliations

Allicin suppresses the migration and invasion in cervical cancer cells mainly by inhibiting NRF2

Qiumei Zhang et al. Exp Ther Med. 2019 Mar.

Retraction in

Abstract

Emerging evidence has demonstrated the antitumor activity of allicin in various tumors. However, little study has been carried out on the functional role of allicin in cervical cancer. Our data showed that allicin suppressed cervical cancer cell viability in a time- and dose-dependent manner. Allicin treatment could reverse H2O2-induced reactive oxygen species accumulation. Meanwhile, levels of glutathione and superoxide dismutase were increased, but malondialdehyde was decreased after allicin incubation for 48 h. Furthermore, TUNEL staining showed that H2O2 treatment induced cell apoptosis, but allicin treatment could decrease cell apoptosis. Western blot assay showed that allicin could suppress the expression of nuclear factor erythroid 2-related factor 2 (NRF2) and heme oxygenase 1. We also showed that NRF2 prompted SiHa cell proliferation and reduced SiHa cell apoptosis. More importantly, allicin-inactivated phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling could be partially reversed by overexpressing of NRF2. We also evaluated cell apoptosis in SiHa cells transfected with plasmid NRF2. Our data showed that allicin-induced cell apoptosis (43.5±3.8%) could largely be abolished by upregulation of NRF2 (12.3±2.08%). In summary, our data showed allicin was effective in suppressing the malignant phenotype of cervical cancer cells mainly by inhibiting the expression of NRF2, showing the potential clinical benefits of allicin in cervical cancer patients.

Keywords: allicin; cervical cancer; nuclear factor erythroid 2-related factor 2; oxidative stress.

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Figures

Figure 1.
Figure 1.
Allicin suppressed SiHa Cell Viability in time- and dose-dependent manner. (A) Treatment with 5, 20 and 50 nM allicin significantly decreased cell viability. (B) incubation of 20 nM allicin reduced SiHa cell viability at 24, 48 and 72 h. *P<0.05, **P<0.01, vs. control.
Figure 2.
Figure 2.
Allicin-induced accumulation of reactive oxygen species and SiHa Cell apoptosis. (A) DHE staining. Quantification of (B) GSH, (C) SOD and (D) MDA contents. (E) TUNEL staining. *P<0.05, **P<0.01, vs. control. DHE, dihydroethidium; GSH, glutathione; SOD, superoxide dismutase; MDA, malondialdehyde; TUNEL, terminal deoxy-nucleotidyl transferase-mediated dUTP nick-end labeling; DMSO, dimethyl sulfoxide; con, control.
Figure 3.
Figure 3.
Treatment with allicin significantly suppressed the level of NRF2 and HO-1. **P<0.01 and ***P<0.001, vs. control. NRF2, nuclear factor erythroid 2-related factor 2; HO-1, heme oxygenase 1.
Figure 4.
Figure 4.
NRF2 prompted SiHa cell proliferation and reduced SiHa cell apoptosis. Overexpressing NRF2 significantly enhanced (A) SiHa cell migration and (B) invasion capacity. (C) Overexpressing NRF2 could largely reverse H2O2-induced cell apoptosis. *P<0.05, **P<0.01 and ***P<0.001, vs. control. P, plasmid; NRF2, nuclear factor erythroid 2-related factor 2.
Figure 5.
Figure 5.
Allicin induced SiHa cell apoptosis mainly by suppressing the expression of NRF2. (A) Western blot assay showed that allicin-inactivated PI3K/AKT signaling could be partially reversed by overexpressing of NRF2. (B) Allicin-induced cell apoptosis could largely be abolished by upregulation of NRF2. *P<0.05, **P<0.01 and ***P<0.001, vs. control. p, plasmid; NRF2, nuclear factor erythroid 2-related factor 2; AKT, protein kinase B; p-AKT, phosphorylated AKT; Bcl-2, B-cell lymphoma 2.
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