scholarly journals Proapoptotic Activity and Chemosensitizing Effect of the Novel Akt Inhibitor (2S)-1-(1H-Indol-3-yl)-3-[5-(3-methyl-2H-indazol-5-yl)pyridin-3-yl]oxypropan2-amine (A443654) in T-Cell Acute Lymphoblastic Leukemia

2008 ◽  
Vol 74 (3) ◽  
pp. 884-895 ◽  
Author(s):  
Federica Falà ◽  
William L. Blalock ◽  
Pier Luigi Tazzari ◽  
Alessandra Cappellini ◽  
Francesca Chiarini ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
The Novel ◽  
Akt Inhibitor ◽  
Cell Acute Lymphoblastic Leukemia

scholarly journals Cytotoxic activity of the novel Akt inhibitor, MK-2206, in T-cell acute lymphoblastic leukemia

Leukemia ◽  
2012 ◽  
Vol 26 (11) ◽  
pp. 2336-2342 ◽  
Author(s):  
C Simioni ◽  
L M Neri ◽  
G Tabellini ◽  
F Ricci ◽  
D Bressanin ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Cytotoxic Activity ◽  
Lymphoblastic Leukemia ◽  
The Novel ◽  
Akt Inhibitor ◽  
Cell Acute Lymphoblastic Leukemia

Preclinical testing of the Akt inhibitor triciribine in T-cell acute lymphoblastic leukemia

2010 ◽  
Vol 226 (3) ◽  
pp. 822-831 ◽  
Author(s):  
Camilla Evangelisti ◽  
Francesca Ricci ◽  
Pierluigi Tazzari ◽  
Francesca Chiarini ◽  
Michela Battistelli ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Akt Inhibitor ◽  
Preclinical Testing ◽  
Cell Acute Lymphoblastic Leukemia

scholarly journals Inhibition of BCL11B induces downregulation of PTK7 and results in growth retardation and apoptosis in T-cell acute lymphoblastic leukemia

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Kehan Li ◽  
Cunte Chen ◽  
Rili Gao ◽  
Xibao Yu ◽  
Youxue Huang ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Growth Retardation ◽  
Lymphoblastic Leukemia ◽  
Downstream Target ◽  
B Cell Leukemia ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Induced Apoptosis ◽  
Necrosis Factor ◽  
Aggressive Subtype

AbstractT-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subtype of leukemia with poor prognosis, and biomarkers and novel therapeutic targets are urgently needed for this disease. Our previous studies have found that inhibition of the B-cell leukemia/lymphoma 11B (BCL11B) gene could significantly promote the apoptosis and growth retardation of T-ALL cells, but the molecular mechanism underlying this effect remains unclear. This study intends to investigate genes downstream of BCL11B and further explore its function in T-ALL cells. We found that PTK7 was a potential downstream target of BCL11B in T-ALL. Compared with the healthy individuals (HIs), PTK7 was overexpressed in T-ALL cells, and BCL11B expression was positively correlated with PTK7 expression. Importantly, BCL11B knockdown reduced PTK7 expression in T-ALL cells. Similar to the effects of BCL11B silencing, downregulation of PTK7 inhibited cell proliferation and induced apoptosis in Molt-4 cells via up-regulating the expression of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and p27. Altogether, our studies suggest that PTK7 is a potential downstream target of BCL11B, and downregulation of PTK7 expression via inhibition of the BCL11B pathway induces growth retardation and apoptosis in T-ALL cells.

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