T-cell acute lymphoblastic leukaemia (T-ALL) is an aggressive haematological malignancy that is characterized by a high frequency of induction failure and by early relapse. Many studies have revealed that metadherin (MTDH) is highly expressed in a variety of malignant solid tumours and plays an important role in the occurrence and development of tumours. However, the relationship between the expression of MTDH and T-ALL has not yet been reported, and the regulatory factors of MTDH are still unknown. Our previous studies found that mPGES-1/PGE2 was important for promoting the growth of leukaemia cells. In the present study, we found that MTDH was highly expressed in primary T-ALL cells and in the Jurkat cell line. Our results showed that mPGES-1/PGE2 regulates the expression of MTDH through the EP3/cAMP/PKA-CREB pathway in T-ALL cells. Downregulation of MTDH inhibits the growth of Jurkat cells in vitro and in vivo. Our results suggest that MTDH could be a potential target for the treatment of T-ALL.

T细胞急性淋巴细胞白血病（T-ALL）是一种侵袭性血液系统恶性肿瘤，其特征在于诱导失败的频率高且早期复发。许多研究表明，metdherin（MTDH）在各种恶性实体瘤中高度表达，并在肿瘤的发生和发展中起重要作用。然而，尚未报道MTDH的表达与T-ALL之间的关系，并且MTDH的调节因子仍是未知的。我们以前的研究发现，mPGES-1 / PGE2对促进白血病细胞的生长很重要。在本研究中，我们发现MTDH在原代T-ALL细胞和Jurkat细胞系中高表达。我们的研究结果表明，mPGES-1 / PGE2通过T3细胞中的EP3 / cAMP / PKA-CREB途径调节MTDH的表达。MTDH的下调在体外和体内抑制Jurkat细胞的生长。我们的结果表明，MTDH可能是治疗T-ALL的潜在靶标。