https://orcid.org/0009-0006-2269-8325
Figures & data
Figure 1. DHA and PDT combined treatment can suppresses cell proliferation and migration. (A) Images of Eca109 and Ec9706 cells treated with DHA or/and PDT, the clony numbers significantly decreased in the DHA + PDT group. (B) Wound healing assay: with the treatment of DHA + PDT, cell migration was inhibited. (C) The protein expression of N-cadherin, E-cadherin, Vimentin was determined by western-bloting analysis.
Figure 2. Combined treatment of DHA and PDT inhibits glycolysis of Eca109 and Ec9706. (A)Glucose uptake: in the control group, DHA alone group or PDT alone group, glucose uptake significant less than DHA + PDT group. (B) Lactate production: in the control group, DHA alone group or PDT alone group, glucose uptake significant more than DHA + PDT group. Control (NC), 80 μmol/ml DHA alone treat (DHA), post PDT 4h alone (PDT), DHA + PDT (P + D). Error bars indicate SD. *p < 0.05, **p < 0.001 by one-way ANOVA with post hoc intergroup comparisons (A,B).
Figure 3. PKM2 is overexpression in oesophageal cancer tissue and DHA enhances PDT sensitivity by inhibiting PKM2. (A)DNA copy number of PKM in the different types of cancer was analysed using GEPIA database. (B) DNA copy number PKM in ESCC was analysed using TCGA. (C) DNA copy number of PKM2 in ESCC was analysed using Oncomine. (D) Western blot analysis for PKM2 expression level in four groups. β-actin was used as an internal control. (E) Western blot analysis for PKM2 expression level in post-PDT 4h alone group, post-PDT 4h + DHA group, post-PDT 24h alone group, post-PDT 24h + DHA group. β-actin was used as an internal control.
Figure 4. Overexpression of PKM2 alleviates the effect of combined treated on cell proliferation and migration. (A) Colony formation on OE-PKM2-Eca109 and OE-PKM2-Ec9706 for cell proliferation via PKM2. (B) Wound healing assay on OE-PKM2-Eca109 and OE-PKM2-Ec9706 for cell migration via PKM2. (C) The protein expression of N-cadherin, E-cadherin, Vimentin was determined by western-bloting analysis for cell migration and invasion via PKM2.
Figure 5. The overexpression of PKM2 influenced the effect of combined treatment on glycolysis.(A) Glucose uptake of OE-PKM2-Eca109 and OE-PKM2-Ec9706 in the control group, DHA group, PDT group and DHA + PDT group were examined.(B) Lactate product of OE-PKM2-Eca109 and OE-PKM2-Ec9706 in the control group, DHA group, PDT group and DHA + PDT group were examined. Control (NC), 80 μmol/ml DHA alone treat (DHA), post PDT 4h alone (PDT), DHA + PDT (P + D). (C) Western blot analysis for PKM2 expression level of OE-PKM2-Eca109 and OE-PKM2-Ec9706 in four groups. β-actin was used as an internal control. (D) Western blot analysis for PKM2 expression level of OE-PKM2-Eca109 and OE-PKM2-Ec9706 in post-PDT 4h alone group, post-PDT 4h + DHA group, post-PDT 24h alone group, post-PDT 24h + DHA group. β-actin was used as an internal control.
Figure 6. Combined treatment of DHA and PDT inhibited glycolysis by down-regulated the expression of PKM2 in vivo. (A) schematic model of DHA + PDT treated-mice. (B) Xenografted tumours were harvested at the end of experiments. (C) Protein expression of PKM2 was detected by immunohistochemistry. (D) Western blot analysis of PKM2, β-actin was used as an internal control. (E) The production of lactate in serum was measured by Lactic Acid Assay kit. Error bars indicate SD. *p < 0.05, **p < 0.001 by one-way ANOVA with post hoc intergroup comparisons.
