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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: PKM2 is the target of proanthocyanidin B2 during the inhibition of hepatocellular carcinoma

Fig. 4

PB2 disrupted the interaction between PKM2/HSP90/HIF-1α in HCC cells. a Western blotting showed that PB2 downregulated the expression of HIF-1α and HSP90 in HCC cells. b The co-immunoprecipitation assay. Both HIF-1α and HSP90 were pulled-down by PKM2. The levels of the PKM2/HIF-1α complex in PB2 groups were lower than those in the normal control (NC) groups, while the levels of PKM2/HSP90 complex in the PB2 groups were higher than those in the NC groups. c The effects of PKM2 overexpression or knockdown on the expression of HIF-1α and HSP90, by western blotting. d PB2 reduced the expression of HIF-1α and HSP90 in PKM2-OE or sh-PKM2 HCC cells when compared to the EV group. e Double-immunofluorescence (IF) staining of HCC cells (original magnification, 400×). PKM2 was stained as red, HIF-1α or HSP90 was stained as green. HSP90 was mainly localized in the cytoplasm of HCC cells, while HIF-1α was localized in the nucleus. The double-IF staining and co-localization suggested that PB2 promoted the co-localization of PKM2/HSP90 in the cytoplasm, while it suppressed the co-localization of PKM2/HIF-1α in the nucleus, which was quantified using Pearson’s co-localization coefficient. f Effects of HIF-1α activator FG-4592 on PB2-treated HCC cells. g Effects of HIF-1α activator FG-4592 and HIF-1α inhibitor BAY87–2243 on PKM2-overexpression or PKM2-knockout HCC cells. *P < 0.05 vs. the NC group (4e: Student’s t-test)

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