Table 2.
Upstream regulators of GLUTs in endometrial cancer.
| Upstream regulators | GLUT1 | GLUT3 | GLUT4 | GLUT6 | Regulatory mechanisms | |
|---|---|---|---|---|---|---|
| Hormones | Estrogen | + | + | ER | ||
| Progesterone | + | PGRMC1, IR | ||||
| High insulin | + | + | IRAP, IGF1R, PI3K/AKT pathway | |||
| High glucose | + | + | + | ER, AMPK/mTOR/S6 pathway | ||
| Hypoxia | + | + | HIF-1α, ATP, HtrA3 | |||
| Cytokines | IL-3/IL-7 | + | PI3K/AKT/mTOR pathway | |||
| TNF-α | + | NF-κB, RELA | ||||
| VEGF | + | / | ||||
| Enzymes | ABHD5 | + | AKT pathway | |||
| ALDH | + | / | ||||
| Natural compounds | Flavonoids | − | / | |||
| Vitamin C | − | HIF-1α | ||||
+, positive regulation; −, negative regulation.
HIF-1α, hypoxia-inducible factor-1α; VEGF, vascular endothelial growth factor; IL-3/IL-7, interleukin 3/7; ABHD5, abhydrolase domain containing 5; ALDH, high-level aldehyde dehydrogenase; Vitamin C, ascorbic acid; ER, estrogen receptor; PGRMC1, the progesterone receptor membrane component 1; IR, insulin receptor; IRAP, insulin-regulated aminopeptidase; IGF1R, insulin-like growth factor 1 receptor; PI3K, phosphatidylinositol 3-kinase; AKT, the serine-threonine kinase; AMPK, adenosine 5′-monophosphate (AMP)-activated protein kinase; mTOR, mammalian target of rapamycin; ATP, adenosine triphosphate; HtrA3, high-temperature requirement A3; NF-κB, nuclear factor kappa-B.