Fig. 2: Overexpressed TGF-βRII inhibited the glycolysis in CAFs and suppressed tumor growth. | Cell Death Discovery

Fig. 2: Overexpressed TGF-βRII inhibited the glycolysis in CAFs and suppressed tumor growth.

From: TGF-βRII regulates glucose metabolism in oral cancer-associated fibroblasts via promoting PKM2 nuclear translocation

Fig. 2

A By immunocyte chemistry staining, TGF-βRII overexpressed in the intervened CAFs, mainly located in the cellular membrane and cytoplasm, while PKM2 and HIF-1α were weakly positive in the controls. B–D Immunoblot showed a reduction of PKM2 and HIF-1α when TGF-βRII was augmented in CAFs. Quantification of TGF-βRII, PKM2, and HIF-1α mRNA or protein levels in CAFs with a significant statistical difference among the groups. E There was no significant statistic between the CAFs with overexpressed TGF-βRII and the controls by MTT assay. F Abundant autophagosomes and mitochondria were observed in the controls while less in the CAFs with overexpressed TGF-βRII under the electron microscope (blue arrows: autophagosomes; red arrows: mitochondria). G Compared to controls, by glucose assay, upregulated TGF-βRII attenuated the glucose uptake in the CAFs. H Less production of lactic acid was detected in the experimental CAFs than the controls with a significant statistical difference. Relative mRNA or protein expression level was quantified after normalization to β-actin. Scale bar = 100 μm. n ≥ 3; error bars, mean ± SD; n.s. not significant, **P < 0.01, ***P < 0.001, ****P < 0.0001; t test.

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