HIF1A and neoplasm: Importantly, as shown in Figures 4f and g, immunofluorescence and immunoprecipitation showed that endogenous Smad3 interacted and co-localized with HIF-1α, which is consistent with previous reports by Rozen-Zvi et al.29 and Shi et al.30 the study also demonstrated that the formation of a Smad3/HIF-1α transcriptional complex led to increase phosphorylation of Smad3,30, 31, 32 which may be a novel interaction in regulation of tumor glycolysis.