Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia

The expression levels of the above mentioned genes and their correlation with the BCL11B gene were analyzed in patients with T-ALL using the TaqMan and SYBR Green I real-time polymerase chain reaction technique.Expression levels of BCL11B, BCL2L1, and CREBBP mRNA in T-ALL patients were significantly higher than those from healthy controls (P < 0.05). In T-ALL patients, the BCL11B expression level was negatively correlated with the BCL2L1 expression level (rs = -0.700; P < 0.05), and positively correlated with the SPP1 expression level (rs = 0.683; P < 0.05). In healthy controls, the BCL11B expression level did not correlate with the TNFSF10, BCL2L1, SPP1, or CREBBP expression levels.Over-expression of BCL11B might play a role in anti-apoptosis in T-ALL cells through up-regulation of its downstream genes BCL2L1 and CREBBP.T-cell acute lymphoblastic leukemia (T-ALL) accounts for 15% of newly diagnosed ALL cases in children and 20-25% of ALL cases in adults [1,2]. Overall, these are aggressive malignancies that do not respond well to chemotherapy and have a poorer prognosis than their B-cell counterparts [3]. The development of targeted therapies, including monoclonal antibodies and gene therapy, continues. Small interfering RNA (siRNA) is a promising gene-targeting agent that has shown great potential, particularly in the field of cancer treatment [4-6].The B-cell chronic lymphocytic leukemia (CLL)/lymphoma 11B (BCL11B) gene plays a crucial role in T-cell development, differentiation, and proliferation [7], and altered expression, mutation, disruption, or rearrangement of BCL11B have been associated with T-cell malignancies [8-11]. BCL11B over-expression has been observed primarily in T-cell malignancies [8,12]. BCL11B has been hypothesized to act as a tumor suppressor gene [9,13], but its precise function remains unclear.BCL2-like 1 (BCL2L1; Bcl-xL) is similar to Bcl-2 because it restrains the apoptosis induction of multiple stimuli, and is a key factor in the termin