Table 1.
Specific Hallmark of Cancer | REDD1 Role | Effect | References |
---|---|---|---|
Evasion from growth inhibition | N/D * | N/D | N/D |
Sustaining proliferation | REDD1 inhibited proliferation in vitro and in vivo | Anti-cancer | [8,18,24,46,49,50,62,63] |
Attenuation of apoptosis | REDD1 expression was correlated with abrogation of apoptosis | Pro-oncogenic | [1,64,65,66,67] |
Stimulation of neo-angiogenesis | REDD1 overexpression was correlated with blood vessel density and slower angiogenesis rate in oral squamous carcinoma | Anti-cancer | [56] |
REDD1 induced angiogenesis in glioblastoma, colon, and lung cancer cells | Pro-oncogenic | [70,71,72,73,74,75,76] | |
Escape from immune response | REDD1 promoted tumor escape from immune system | Pro-oncogenic | [73,80] |
Immortalization | N/D | N/D | N/D |
Tumor-associated inflammation | REDD1 deficiency blunted response to LPS, attenuated production of pro-inflammatory cytokines, and reduced inflammation | Pro-oncogenic | [94,95] |
Genetic instability | N/D | N/D | N/D |
Invasion and metastasis | REDD1 overexpression in TAM was associated with metastasis induction | Pro-oncogenic | [55,78] |
Metabolic shift | REDD1 depleted intracellular ATP, stimulated ROS-mediated cytotoxicity, and decreased glucose uptake | Anti-cancer | [18,20,21,22] |
Cell senescence | REDD1 promoted pro-survival autophagy in thymocytes | Pro-oncogenic | [64,87] |
Cellular plasticity | REDD1 overexpression blocked keratinocyte differentiation | Pro-oncogenic | [1,18] |
Non-mutational epigenetic reprogramming | REDD1 may cause changes in methylation pattern | Questionable | [88] |
Microbiome polymorphism | N/D | N/D | N/D |
* N/D, not described.