Rapamycin suppresses small bowel adenocarcinoma HUTU 80 cells proliferation by inhibiting hypoxia-inducible factor-1α mediated metabolic reprogramming

Figure 4 RNA sequencing results of rapamycin treatment with HUTU 80 cells. A: Volcano plot showed the number of differentially expressed genes (DEGs) in the rapamycin (RAPA) group and the control group; B: Gene Ontology enrichment analysis related to antitumor functions; C: Selection of the top 10 Kyoto Encyclopedia of Genes and Genomes pathways related to antitumor effects; D: Heatmap displayed DEGs involved in the hypoxia-inducible factor (HIF)-1α and glycolysis/gluconeogenesis pathways; E: Quantitative polymerase chain reaction was used to detect the messenger RNA expression levels of HIF-1α, PDK1, LDHA and VEGF in RAPA-treated HUTU 80 cells. Data are presented as the mean ± SD (n = 3). ^aP < 0.05. ^bP < 0.01. ^cP < 0.001. RAPA: Rapamycin; MF: Molecular function; CC: Cellular component; BP: Biological process; ECM: Extracellular matrix; MAPK: Mitogen-activated protein kinase; PI3K/Akt: Phosphatidylinositol 3-kinase/protein kinase B; JAK/STAT: Janus tyrosine kinase/signal transducer and activator of transcription; mTOR: Mammalian target of rapamycin; AMPK: Adenosine 5’-monophosphate-activated protein kinase; HIF-1α: Hypoxia-inducible factor-1α; mRNA: Messenger RNA.