Melatonin Inhibits Reactive Oxygen Species-Driven Proliferation, Epithelial-Mesenchymal Transition, and Vasculogenic Mimicry in Oral Cancer

Figure 5

Melatonin hampered oral cancer tumorigenesis in vivo. SCID mice were subcutaneously injected with 2 × 10⁶ Cal27 cells. After 7 days, the animals received intraperitoneally melatonin or the vehicle (control) five days a week in a span of three weeks. All the mice were sacrificed under euthanasia six weeks after tumor cell implantation. (a) Representative images of tumors from the two groups. (b) Tumor volume was measured and calculated once a week for six weeks. (c) Tumor weight was measured. (d) ROS level was measured in the tumor tissues. (e) Western blot results of p-Akt, Akt, p-ERK, ERK, E-cadherin, Vimentin, cyclin D1, PCNA, Bcl-2, Bax, Snail, HIF-1α, and VEGF in the tumor tissues. GAPDH was used as endogenous control. The ratios from the indicated proteins to GAPDH are indicated below the bands. (f) IHC assays were performed to evaluate the levels of p-Akt, p-ERK, E-cadherin, Vimentin, cyclin D1, PCNA, Bcl-2, Bax, Snail, HIF-1α, and VEGF in the tumor tissues. Data are represented as the mean ± SD of three independent experiments. , versus control group. Ctrl: control; Mel: melatonin; NAC: N-acetyl-L-cysteine.

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