scholarly journals A Sanctuary for cancer cells: Microenvironment in T-cell acute lymphoblastic leukemia survival and drug resistance

2017 ◽  
Vol 1 (2) ◽  
Author(s):  
Filomena Di Giacomo ◽  
Danilo Fiore ◽  
Peter W. Kyriakides ◽  
Giorgio Inghirami
Keyword(s):  
Drug Resistance ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Cancer Cells ◽  
Lymphoblastic Leukemia ◽  
Cell Acute Lymphoblastic Leukemia

scholarly journals NHE1 has a notable role in metastasis and drug resistance of T-cell acute lymphoblastic leukemia

2017 ◽  
Vol 14 (4) ◽  
pp. 4256-4262 ◽  
Author(s):  
Ehtisham Altaf ◽  
Xiaoxing Huang ◽  
Jie Xiong ◽  
Xiangyong Yang ◽  
Xinzhou Deng ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Cell Acute Lymphoblastic Leukemia

Modular domains within a super enhancer determine drug resistance in T-cell acute lymphoblastic leukemia

2016 ◽  
Vol 44 (9) ◽  
pp. S25
Author(s):  
Warren Pear ◽  
Yumi Yashiro-Ohtani ◽  
Jelena Petrovic ◽  
Shuqian Yu ◽  
Vicki Mercado ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Super Enhancer ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Modular Domains

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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