It is bound to micro RNA (miR)-29a-3p in a targeted manner. and the expression level of miR-29a-3p in AML patients was prominently lower than that in normal controls.
Acute myeloid leukemia (AML) is a heterogeneous disease with different clinical course and prognosis. microRNA-29 (miR-29) family of non-coding small RNAs can play an important role in pathogenesis of AML, but also can influence response to therapy.The purpose of the study was to evaluate miR-29c expression in AML patients in relationship to clinical parameters and response to chemotherapy, including azacitidine.
Among them miR-29a and miR-142-3p were selectively encountered in Northern blot analysis and their significantly decreased expression in AML was further confirmed.
A significant decrease of miR-29a and 142-3p levels and an obvious increase in their target protein levels were also observed in blasts from acute myeloid leukemia.
Furthermore, our data showed that deregulated expression of tumor suppressor microRNAs, such as miR-29a and miR-30c, might contribute to sensitivity to cytarabine, which is observed in NPM1 mutated acute myeloid leukemia.
In conclusion, up-regulation of Ski in AML with -7/del7q is caused by loss of miR-29a. miR-29a may therefore function as an important tumor suppressor in AML by restraining expression of the SKI oncogene.
Our data indicate that miR-29a regulates early hematopoiesis and suggest that miR-29a initiates AML by converting myeloid progenitors into self-renewing LSC.