Cell Death Dis：mPGES-1/PGE2/MTDH轴调控T-ALL细胞生长

Acute lymphoblastic leukemia is a highly heterogeneous aggressive hematologic malignancy that affects about one in every 100,000 adultsDespite the very similar treatment strategies, The prognosis of T-cell acute lymphoblastic leukemia (T-ALL) is much worse than that of B-cell acute lymphoblastic leukemia (B-ALL), due to the high rate of treatment failure and early recurrenceMany studies have shown that MTDH (metherherin) is highly expressed in various malignant solid tumors and plays an important role in the development of tumorsHowever, the relationship between MTDH expression levels and T-ALL is not clear, and the adjustment factors of MTDH are still unknownresearchers have previously found that the mPGES-1/PGE2 signaling pathway is critical to promoting the growth of leukemia cellsmPGES-1 is an end-to-end enzyme responsible for converting COX (epoxy) derived From PGH2 (Prostagland h2) into PGE2 (Prostaglandin E2)In this study, researchers confirmed for the first time the high expression of mPGES-1 in human leukemia progeny cells and acute myeloid leukemia cell lines HL-60 and K562MTDH is also highly expressed in the primary T-ALL cell and Jurkat cell linesFurther studiesfound that mPGES-1/PGE2 can regulate the expression of MTDH by mediatating ep3/cAMP/PKA-CREB signaling pathways in T-ALL cellsThe reduction of MTDH expression level inhibits the growth of Jurkat cellscomprehensive results show that MTDH may be a potential target for the treatment of T-ALL, and targeting MTDH and its regulatory signaling pathways may be an effective strategy for treating T-ALL