|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overall, these data indicate that miR-125b-5p played a role in the suppressive effect on BCa by targeting HK2 through suppressing PI3K/AKT pathway and offer a potential therapeutic target for BCa.
|
31605287 |
2020 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overexpression of KIFC1 phosphorylated GSK3β and promoted Snail through activating AKT (protein kinase B0) to induce proliferation and epithelial-mesenchymal transition (EMT) and, therefore, substantially promoted BC migration and metastasis.
|
31278883 |
2019 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, miR-328-3p inhibited epithelial-mesenchymal transition (EMT) and inactivated PI3K/AKT pathway in BC.
|
31298367 |
2019 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this context, PIK3CA, p-AKT and nuclear PTEN could be used along with other biomarkers for prognosis and selection of appropriate therapy in the clinical management of bladder cancer.
|
30941989 |
2019 |
|
Bladder Neoplasm
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Besides, miR-15 regulated epithelial-mesenchymal transition (EMT)-related makers, protein kinase B (AKT), and the phosphorylation of AKT protein levels in BC using the Western blot assay.
|
31696468 |
2019 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Immunofluorescence staining, flow cytometry analysis and treatment with an AKT inhibitor were performed to explore the molecular regulation mechanisms of TEF in BC.
|
30515906 |
2019 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
RASAL2 inhibits tumor angiogenesis via p-AKT/ETS1 signaling in bladder cancer.
|
29702203 |
2018 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Further, transwell chambers assay showed that GA suppressed bladder cancer cell invasion and migration through p-AKT/MMP-2 signaling pathway.
|
29567231 |
2018 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
We discovered a positive feedback loop, in which the activation of p38 and AKT downstream from the altered FGFR3 upregulates <i>MYC</i> mRNA levels and stabilizes MYC protein, respectively, leading to the accumulation of MYC, which directly upregulates <i>FGFR3</i> expression by binding to active enhancers upstream from <i>FGFR3</i> Disruption of this FGFR3/MYC loop in bladder cancer cell lines by treatment with FGFR3, p38, AKT, or BET bromodomain inhibitors (JQ1) preventing <i>MYC</i> transcription decreased cell viability <i>in vitro</i> and tumor growth <i>in vivo</i> A relevance of this loop to human bladder tumors was supported by the positive correlation between <i>FGFR3</i> and <i>MYC</i> levels in tumors bearing <i>FGFR3</i> mutations, and the decrease in FGFR3 and MYC levels following anti-FGFR treatment in a PDX model bearing an <i>FGFR3</i> mutation.
|
29463565 |
2018 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Deregulation of the PI3K/AKT/mTOR pathway was observed in more than 40% of bladder tumors and suggested the use of mTOR as a target for the treatment of urothelial cancers.
|
29454321 |
2018 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, our study illustrated a novel signaling cascade of LINC00641/miR-197-3p/KLF10/PTEN/PI3K/AKT pathway regulating bladder cancer development.
|
30060954 |
2018 |
|
Bladder Neoplasm
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The <i>AKT1</i> rs2498801 variant is associated with a decreased risk of BC (OR=0.57, 95 % CI=0.39-0.82, p=0.003, AG vs AA; OR=0.74, 95 % CI=0.56-0.97, p=0.032, G vs A) while, AKT1 rs1130233 polymorphism considerably increased the risk of BC (OR=3.70, 95 % CI=2.52-5.43, p<0.0001, GA vs GG; OR=5.81, 95 % CI=1.53-21.97, p=0.010, AA vs GG; OR=2.71, 95 % CI=1.98-3.70, p<0.0001, A vs G).
|
29383014 |
2018 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Modulation of G6PD affects bladder cancer via ROS accumulation and the AKT pathway in vitro.
|
30066842 |
2018 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Targeting the PI3K/AKT/mTOR Pathway in Bladder Cancer.
|
28889395 |
2018 |
|
Bladder Neoplasm
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In the present study, the expression of the AKT serine/threonine kinase (AKT) signaling pathway in bladder cancer and normal bladder tissue was investigated, and the influence of β-elemene on bladder cancer cells and the mechanisms involved were assessed.
|
30333873 |
2018 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
MicroRNA-608 inhibits proliferation of bladder cancer via AKT/FOXO3a signaling pathway.
|
28549468 |
2017 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Actein induces autophagy and apoptosis in human bladder cancer by potentiating ROS/JNK and inhibiting AKT pathways.
|
29348843 |
2017 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Moreover, CCDC34 silencing decreased the phosphorylation of MEK, ERK1/2, JNK, p38 and Akt, and the expressions of c-Raf and c-Jun, indicating MAPK and AKT pathways (ERK/MAPK, p38/MAPK, JNK/MAPK and PI3K/Akt) might be involved in CCDC34 regulation of bladder cancer cell proliferation and migration.
|
26312564 |
2015 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, these findings highlight for the first time that ANG could play a pivotal role in the development of bladder cancer through regulating AKT/mTOR signaling pathway.
|
25564356 |
2015 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data provide important clues on the therapeutic benefits of targeting Akt1 for bladder cancer therapy.
|
26148825 |
2015 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, GOLPH3 is likely to play important roles in bladder cancer progression via modulating AKT/mTOR signaling, and it is a novel prognostic biomarker and promising therapeutic target for bladder cancer.
|
26375441 |
2015 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
Manipulating the expression of mutant or wild-type PIK3CA or DUSP1 confirmed that this mechanism is responsible for the induction of apoptosis and the inhibition of tumour proliferation in vitro and in vivo, to sensitise cells to AKT target therapy.Conclusion or interpretation:PIK3CA mutations confer sensitivity to AKT target therapy in BLCA by regulating DUSP1 expression and subsequent ERK1/2 dephosphorylation and can potentially serve as a stratifying biomarker for treatment.
|
25349966 |
2014 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
The PI3K/AKT pathway is considered to play a major role in bladder carcinogenesis, but its relationships with other molecular alterations observed in bladder cancer remain unknown.
|
24122582 |
2014 |
|
Bladder Neoplasm
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Mechanism studies suggest that ERα could control the expression of INPP4B to reduce AKT activity and consequently reduce BCa cell growth.
|
25277204 |
2014 |
|
Bladder Neoplasm
|
0.100 |
Biomarker
|
disease |
BEFREE |
AIB1 predicts bladder cancer outcome and promotes bladder cancer cell proliferation through AKT and E2F1.
|
23511556 |
2013 |