Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The results of Western blot assay showed that the PI3K/AKT/mTOR signaling pathway was activated in bone marrow specimens of patients with MM. miR-215-5p was found to negatively correlate with runt-related transcription factor 1 (RUNX1) expression in MM clinical bone marrow samples.
|
31498483 |
2020 |
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Treatment of cells with specific PI3K inhibitors already used in the clinic reduced myeloma cell adhesion to the bone marrow.
|
31148590 |
2020 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
Biomarker
|
disease |
BEFREE |
These findings indicated the critical roles of ABCG2 and PI3K/AKT signaling in controlling stemness of MM cells, and suggested a novel strategy for targeting ABCG2 and PI3K/AKT signaling to treat MM with MDR.
|
30664164 |
2019 |
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 |
Biomarker
|
disease |
BEFREE |
The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) is such a pathway that is aberrantly activated in a large proportion of MM patients through numerous mechanisms and can play a role in resistance to several existing therapies making this a central pathway in MM pathophysiology.
|
29322846 |
2018 |
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 |
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 |
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 |
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 |
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 |
Using a combination of short hairpin RNA (shRNA) lentivirus-mediated knockdown and pharmacologic isoform-specific inhibition we investigated the role of the PI3K p110γ (PI3Kγ) subunit in regulating MM proliferation and bone marrow microenvironment-induced MM interactions.
|
28282033 |
2017 |
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 |
The Role of PI3K Isoforms in Regulating Bone Marrow Microenvironment Signaling Focusing on Acute Myeloid Leukemia and Multiple Myeloma.
|
28350342 |
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 |
These results indicate that CIP2A modulates myeloma cell proliferation and apoptosis via PI3K/AKT/mTOR signaling and suggest that it can potentially serve as a drug target for the treatment of multiple myeloma.
|
27144172 |
2016 |
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results collectively demonstrate that acid activates the TRPV1-PI3K-Akt-Sp1 signaling in MM cells while inducing HDAC-mediated gene repression, and suggest that a positive feedback loop between acid sensing and the PI3K-Akt signaling is formed in MM cells, leading to MM cell response to acidic bone lesions.
|
27626482 |
2016 |
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 |
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 |