First author | Journal (year) | Results | Function of REDD1 | Tumortype |
---|---|---|---|---|
Horak P | Proc Natl Acad Sci U S A. (2010) [4] | • REDD1 inactivation induces ROS dysregulation and consequent HIF-1α induction that promotes tumorigenesis. • Loss of REDD1 induces a hypoxia-dependent increase in proliferation and anchorage-independent growth in vitro. • Breast carcinomas exhibit silencing of REDD1 expression compared with normal epithelia. | Suppresses tumorigenesis | breast cancer |
Kucejova B | Mol Cancer Res. (2011) [18] | • REDD1 is highly expressed in VHL-deficient clear-cell renal cell carcinoma (ccRCC). • Mutations in REDD1 may contribute to ccRCC development. | possibly a tumor suppressor in sporadic ccRCC. | ccRCC |
Jin HO | Cancer Lett. (2013) [19] | • Sustained overexpression of Redd1 leads to mTORC1 inhibition and to consequent Akt activation that is involved in cell survival. • Akt phosphorylation, which consequent to mTORC1 inhibition and sustained REDD1 overexpression, plays a role in cell survival and resistance to chemotherapeutic drugs. | / | lung cancer cells. |
Zeng Q | Clin Cancer Res. (2018) [20] | • The significant increase of REDD1 expression is detected in bladder urothelial carcinoma(BUC) tissue. • REDD1 is an independent prognostic factor in BUC patients. • Silencing REDD1 expression in T24 and EJ cells decreased cell proliferation, increased apoptosis, and decreased autophagy. The ectopic expression of REDD1 in RT4 and BIU87 cells had the opposite effect. • Inhibited REDD1 expression sensitizes BUC tumor cells to paclitaxel in a subcutaneous transplant sarcoma model in vivo. | REDD1 is an oncogene. Antagonizing REDD1 could be a potential therapeutic strategy to sensitize BUC cells to paclitaxel | BUC |