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T-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.   Supplementary Information  The online version contains supplementary material available at 10.1186/s40364-021-00270-3.

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