Cellular hypoxia reprograms drug response and reveals curcumin-driven cancer stem-cell-associated marker enrichment in oral squamous cell carcinoma

Figure 1 Expression of hypoxia-induced factor 1 alpha in OECM-1 cells grown under normoxic and hypoxic conditions. Statistical analysis was performed using an unpaired t-test. ^aP = 0.0032, comparison between normoxic and hypoxic groups.

Figure 2 Treatment induced cytotoxicity in OECM-1 cells under normoxic and hypoxic conditions. A: Single treatments of increasing concentrations of carboplatin and curcumin under normoxia; B: Single treatments of increasing concentrations of carboplatin and curcumin under hypoxia; C: Combination treatment with increasing doses of curcumin and fixed 0.1 mmol/L carboplatin under normoxia; D: Combination treatment with increasing doses of curcumin and fixed 0.1 mmol/L carboplatin under hypoxia.

Figure 3 Total reactive oxygen species levels in live OECM-1 cells after treatment with carboplatin, curcumin, and curcumin combined with carboplatin under normoxic and hypoxic conditions. A: Normoxia; B: Hypoxia. Statistical analysis was performed using one-way ANOVA with Tukey’s multiple comparison test. ^aP < 0.0001, ^bP = 0.039, ^cP = 0.004, ^dP < 0.0001. ROS: Reactive oxygen species.

Figure 4 Apoptotic induction of OECM-1 cells after treatment with carboplatin, curcumin, and curcumin combined with carboplatin under normoxic and hypoxic conditions. A: Normoxia; B: Hypoxia.

Figure 5 Stem cell surface marker expression in OECM-1 cells treated with carboplatin, curcumin, and curcumin combined with carboplatin under normoxic and hypoxic conditions. A: Normoxia; B: Hypoxia. Statistical analysis was performed using two-way ANOVA with Tukey’s multiple comparison test.