|First author||Journal (year)||Results||Function of REDD1||Tumortype|
|Horak P||Proc Natl Acad Sci U S A. (2010) ||
• 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) ||
• 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) ||
• 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) ||
• 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