miR-21 mediates hematopoietic suppression in MDS by activating TGF-β signaling

Author:

Bhagat Tushar D.1,Zhou Li1,Sokol Lubomir2,Kessel Rachel1,Caceres Gisela2,Gundabolu Krishna1,Tamari Roni1,Gordon Shanisha1,Mantzaris Ioannis1,Jodlowski Tomasz1,Yu Yiting1,Jing Xiaohong1,Polineni Rahul1,Bhatia Kavi1,Pellagatti Andrea3,Boultwood Jacqueline3,Kambhampati Suman4,Steidl Ulrich1,Stein Cy1,Ju Wenjun5,Liu Gang6,Kenny Paraic1,List Alan2,Bitzer Markus15,Verma Amit1

Affiliation:

1. Albert Einstein College of Medicine, Bronx, NY;

2. Moffitt Cancer Center, Tampa, FL;

3. LLR Molecular Haematology Unit, NDCLS, John Radcliffe Hospital, Oxford, UK;

4. VA Medical Center/University of Kansas Medical Center, Kansas City, MO;

5. University of Michigan, Ann Arbor, MI; and

6. University of Alabama, Birmingham, AL

Abstract

Key PointsWe observed that SMAD7, a negative regulator of TGF-β receptor-I kinase, is markedly reduced in MDS, and leads to ineffective hematopoiesis. Increased levels of microRNA-21 are seen in MDS and reduce SMAD7 levels, thus overactivating TGF-β signaling.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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