|
Reperfusion Injury
|
0.300 |
Biomarker
|
disease |
CTD_human |
Modulation of proline-rich akt substrate survival signaling pathways by oxidative stress in mouse brains after transient focal cerebral ischemia.
|
16397181 |
2006 |
|
Carcinogenesis
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
These results suggest that 14-3-3η may be involved in promoting tumorigenesis in pituitary oncocytoma by interacting with PRAS40 (T246) via the mTOR signaling pathway.
|
31849836 |
2019 |
|
melanoma
|
0.040 |
Biomarker
|
disease |
BEFREE |
In addition, the functional role of key Akt pathway members such as PRAS40, GSK3 kinases, WEE1 kinase in melanoma development are discussed together with strategies to modulate these targets.
|
28064546 |
2017 |
|
melanoma
|
0.040 |
Biomarker
|
disease |
BEFREE |
PRAS40 plays an important role in metabolic disorders and multiple cancers, and the phosphorylation of PRAS40 is often associated with the tumor progression of melanoma, prostate cancer, etc.
|
28978182 |
2017 |
|
melanoma
|
0.040 |
AlteredExpression
|
disease |
BEFREE |
Here PRAS40 overexpression in lung adenocarcinoma and cutaneous melanoma was significantly correlated to worse prognosis.
|
28945219 |
2017 |
|
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
Herein, we provide an overview on current understandings of PRAS40 signaling in the tumor formation and progression, which suggests that PRAS40 or phospho-PRAS40 could become a novel biomarker and therapeutic target in tumor.
|
28978182 |
2017 |
|
Carcinogenesis
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
PRAS40 promotes tumorigenesis by deregulating cellular proliferation, apoptosis, senescence, metastasis, etc.
|
28978182 |
2017 |
|
Neoplasms
|
0.040 |
AlteredExpression
|
group |
BEFREE |
Fate mapping studies following transient expression of PRAS40 demonstrated that mTORC1(low) T cells made no contribution to initial tumor control but instead survived to become memory cells proficient in generating recall immunity.
|
25904681 |
2015 |
|
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
Together, these findings reveal a critical role of PRAS40 as an integrator of mTORC1 and AKT signaling for 4E-BP1-mediated translational regulation of tumor cell growth and motility, and highlight PRAS40 phosphorylation as a potential biomarker to evaluate the therapeutic response to mTOR/AKT inhibitors.
|
25961827 |
2015 |
|
melanoma
|
0.040 |
Biomarker
|
disease |
BEFREE |
PRAS40 deregulates apoptosis in malignant melanoma.
|
17440074 |
2007 |
|
Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
Targeting PRAS40 or upstream Akt3 similarly reduced anchorage-independent growth in culture and inhibited tumor development in mice.
|
17440074 |
2007 |
|
Carcinogenesis
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
In this study, PRAS40 was identified as an Akt3 substrate that deregulated apoptosis to promote melanoma tumorigenesis.
|
17440074 |
2007 |
|
Carcinogenesis
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
Expression of proline-rich Akt-substrate PRAS40 in cell survival pathway and carcinogenesis.
|
16174443 |
2005 |
|
Malignant Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
These findings may help elucidate the pleiotropic functions of PRAS40 in cells and suggest a novel therapeutic strategy in cancer patients with high expression of PRAS40 and NF-κB.
|
28945219 |
2017 |
|
Tumor Progression
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
PRAS40 plays an important role in metabolic disorders and multiple cancers, and the phosphorylation of PRAS40 is often associated with the tumor progression of melanoma, prostate cancer, etc.
|
28978182 |
2017 |
|
Primary malignant neoplasm
|
0.030 |
Biomarker
|
group |
BEFREE |
These findings may help elucidate the pleiotropic functions of PRAS40 in cells and suggest a novel therapeutic strategy in cancer patients with high expression of PRAS40 and NF-κB.
|
28945219 |
2017 |
|
Malignant Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
Additionally, we probed new datasets extracted from Oncomine, a cancer microarray database containing datasets derived from patient samples, to further understand the role of PRAS40 (AKT1S1).
|
26003731 |
2015 |
|
Tumor Progression
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
This review discusses the role of PRAS40 and possible feedback mechanisms, and alterations in AKT/PRAS40/mTOR signaling that have been implicated in the pathogenesis of tumor progression.
|
26003731 |
2015 |
|
Primary malignant neoplasm
|
0.030 |
Biomarker
|
group |
BEFREE |
Additionally, we probed new datasets extracted from Oncomine, a cancer microarray database containing datasets derived from patient samples, to further understand the role of PRAS40 (AKT1S1).
|
26003731 |
2015 |
|
Malignant Neoplasms
|
0.030 |
AlteredExpression
|
group |
BEFREE |
The expression of PRAS40, Akt, Raf and 14-3-3 in normal cells and cancer cell lines was determined by Western blot.
|
16174443 |
2005 |
|
Tumor Progression
|
0.030 |
Biomarker
|
phenotype |
BEFREE |
To study the expression of proline-rich Akt-substrate PRAS40 in the cell survival pathway and tumor progression.
|
16174443 |
2005 |
|
Primary malignant neoplasm
|
0.030 |
AlteredExpression
|
group |
BEFREE |
The expression of PRAS40, Akt, Raf and 14-3-3 in normal cells and cancer cell lines was determined by Western blot.
|
16174443 |
2005 |
|
Malignant neoplasm of breast
|
0.020 |
PosttranslationalModification
|
disease |
BEFREE |
GDC-0068 decreased cell viability, induced apoptosis, and inhibited phosphorylation of proline rich Akt substrate 40 kDa and p70 S6 kinase in a dose-dependent manner in PIK3CA-mutant breast cancer brain metastatic cell lines compared with PIK3CA-wildtype cell lines.
|
31173106 |
2019 |
|
Breast Carcinoma
|
0.020 |
PosttranslationalModification
|
disease |
BEFREE |
GDC-0068 decreased cell viability, induced apoptosis, and inhibited phosphorylation of proline rich Akt substrate 40 kDa and p70 S6 kinase in a dose-dependent manner in PIK3CA-mutant breast cancer brain metastatic cell lines compared with PIK3CA-wildtype cell lines.
|
31173106 |
2019 |
|
Non-Small Cell Lung Carcinoma
|
0.020 |
Biomarker
|
disease |
BEFREE |
Our results showed that AKT1 substrate 1 (AKT1S1), a newly proven suppressor of the RP-p53 pathway, was a target of miR-1908, suggesting a probable mechanism for miR-191 suppressing NSCLC cell proliferation.
|
27178817 |
2016 |