|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
2,4-Dihydroxy-3'-methoxy-4'-ethoxychalcone suppresses cell proliferation and induces apoptosis of multiple myeloma <i>via</i> the PI3K/akt/mTOR signaling pathway.
|
31564190 |
2019 |
|
Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Multiple myeloma (MM) is a generally fatal plasma cell cancer that often shows activation of the phosphoinositide 3-kinase/Akt (PI3K/Akt) pathway.
|
25837824 |
2015 |
|
Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Myeloma-secreted 2DDR bound to integrin αVβ3/α5β1 in the progenitors, activated PI3K (phosphoinositide 3-kinase)/Akt signaling, and increased DNMT3A (DNA methyltransferase 3A) expression, resulting in hypermethylation of RUNX2, osterix, and IRF8 This study elucidates an important mechanism for myeloma-induced bone lesions, suggesting that targeting TP may be a viable approach to healing resorbed bone in patients.
|
27559096 |
2016 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
PI3K/p110{delta} is a novel therapeutic target in multiple myeloma.
|
20505158 |
2010 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
A previous study indicated that BENC-511 acted on multiple myeloma and that it had a toxicity by inhibiting the PI3K/protein kinase B (Akt) pathway.
|
30867372 |
2019 |
|
Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
A transcriptional-dependent (TFEB) and independent (PI3K/mTORC1) activation of autophagy mediated FK866 MM cytotoxicity.
|
22955917 |
2012 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Both the ubiquitin proteasome system (UPS) and the PI3K/Akt/mTOR signaling pathways have been implicated in the pathogenesis, and treatment of MM and different lines of evidence suggest a close cross talk between these central cell-regulatory signaling networks.
|
30712673 |
2019 |
|
Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Cancers like multiple myeloma (MM), which display elevated activity in key translation regulatory nodes, such as the PI3K/mammalian target of rapamycin and MYC-eukaryotic initiation factor (eIF) 4E pathways, are predicted to be particularly sensitive to therapeutic strategies that target this process.
|
25197055 |
2014 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Concomitant pan-Raf/PI3K inhibition was also effective in carfilzomib- and lenalidomide-resistant MM models underscoring that this attractive therapeutic anti-MM strategy is suitable for immediate clinical translation.
|
27686868 |
2017 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Endoplasmic reticulum stress induces autophagy and apoptosis while inhibiting proliferation and drug resistance in multiple myeloma through the PI3K/Akt/mTOR signaling pathway.
|
28977849 |
2017 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, our results demonstrated that the enforced expression of miR-145 in H929 cells profoundly decreased the levels of p-AKT and p-PI3K, which may contribute to some extent to the inhibition of MM cell proliferation and survival.
|
25369735 |
2015 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we investigated the effect of miR-20a on the PTEN/PI3K/Akt signaling pathway during MM cell proliferation, migration and apoptosis.
|
29963125 |
2018 |
|
Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Highly expressed NEAT1 promoted cell proliferation through activation of PI3K/AKT pathway, thus participating in the development of MM.
|
30338809 |
2018 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, bortezomib activates the phosphatidylinositol 3-kinase/AKT (PI3K/AKT) pathway (which is essential to the development of myeloma), often resulting in drug resistance and disease recurrence.
|
27439454 |
2017 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
It was observed that FT enhanced the apoptosis caused by bortezomib (Bor) and mitigated proliferation in MM cells, and these events are regulated by nuclear factor-κB (NF-κB), phosphatidylinositol 3-kinase (PI3K)/AKT, and activator protein-1 (AP-1) activation.
|
31284669 |
2019 |
|
Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Moreover, miR-30d carries out its antitumor role in U266 cells through the inhibition of the activation of the PI3K/Akt signaling pathway by negatively regulating MTDH, which reveals its potential for use as a therapeutic target for MM.
|
30132507 |
2018 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Moreover, the novel specific PI3K/Akt/mTOR signaling inhibitor S14161 displayed its prowess as a potential therapeutic agent by targeting MM SP cells.
|
25915427 |
2015 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Noteworthy, the results of the synergistic experiments also revealed that BKM120 could produce a synergistic anti-cancer effect with carfilzomib (CFZ) and provided an enhanced therapeutic efficacy in MM cells, highlighting that PI3K inhibition might be a befitting approach in MM both in mono and combined therapy.
|
30401630 |
2019 |
|
Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Oscillating expression of interleukin-16 in multiple myeloma is associated with proliferation, clonogenic growth, and PI3K/NFKB/MAPK activation.
|
28512269 |
2017 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Polycomb repressive complex 2 (PRC2) components, EZH2 and its homolog EZH1, and PI3K/Akt signaling pathway are focal points as therapeutic targets for multiple myeloma.
|
31571328 |
2019 |
|
Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Previously we showed that tetraspanin overexpression in MM cell lines attenuated mTOR and PI3K cascades, induced protein synthesis, activated unfolded protein response (UPR), and caused autophagic death, all suggesting breach of proteostasis.
|
25422161 |
2015 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Since PTEN-null myeloma lines exhibited much stronger Akt activation than PTEN-expressing cells in response to insulin-like growth factor I stimulation, we determined whether Akt could be responsible for PI3K-mediated cell survival and growth of PTEN-null myeloma lines.
|
13679867 |
2003 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The PI3K/Akt/mTOR signal transduction pathway plays a central role in multiple myeloma (MM) disease progression and development of therapeutic resistance. mTORC1 inhibitors have shown limited efficacy in the clinic, largely attributed to the reactivation of Akt due to rapamycin induced mTORC2 activity.
|
23185517 |
2012 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The PI3K/mTOR/AKT pathway is an integral regulator of survival and drug resistance in multiple myeloma (MM).
|
29254208 |
2017 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The PI3K/Akt/mTOR pathway is constitutively activated in human multiple myeloma (MM) cell lines and in freshly isolated plasmocytes from patients with MM.
|
30787971 |
2019 |