miR-328 Functions as an RNA Decoy to Modulate hnRNP E2 Regulation of mRNA Translation in Leukemic Blasts

نویسندگان

  • Anna M. Eiring
  • Jason G. Harb
  • Paolo Neviani
  • Christopher Garton
  • Joshua J. Oaks
  • Riccardo Spizzo
  • Shujun Liu
  • Sebastian Schwind
  • Ramasamy Santhanam
  • Christopher J. Hickey
  • Heiko Becker
  • Jason C. Chandler
  • Raul Andino
  • Jorge Cortes
  • Peter Hokland
  • Claudia S. Huettner
  • Ravi Bhatia
  • Denis C. Roy
  • Stephen A. Liebhaber
  • Michael A. Caligiuri
  • Guido Marcucci
  • Ramiro Garzon
  • Carlo M. Croce
  • George A. Calin
  • Danilo Perrotti
چکیده

MicroRNAs and heterogeneous ribonucleoproteins (hnRNPs) are posttranscriptional gene regulators that bind mRNA in a sequence-specific manner. Here, we report that loss of miR-328 occurs in blast crisis chronic myelogenous leukemia (CML-BC) in a BCR/ABL dose- and kinase-dependent manner through the MAPK-hnRNP E2 pathway. Restoration of miR-328 expression rescues differentiation and impairs survival of leukemic blasts by simultaneously interacting with the translational regulator poly(rC)-binding protein hnRNP E2 and with the mRNA encoding the survival factor PIM1, respectively. The interaction with hnRNP E2 is independent of the microRNA's seed sequence and it leads to release of CEBPA mRNA from hnRNP E2-mediated translational inhibition. Altogether, these data reveal the dual ability of a microRNA to control cell fate both through base pairing with mRNA targets and through a decoy activity that interferes with the function of regulatory proteins.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

UPF1 regulates myeloid cell functions and S100A9 expression by the hnRNP E2/miRNA-328 balance

UPF1 is a key player in nonsense mediated mRNA decay (NMD) but also involved in posttranscriptional gene regulation. In this study we found that UPF1 regulates the expression of genes with functions in inflammation and myeloid cell differentiation via hnRNP E2. The majority of the UPF1-regulated genes identified in monocytic cells contain a binding site for hnRNP E2 within 5' UTR located intron...

متن کامل

Interplay between miR-574-3p and hnRNP L regulates VEGFA mRNA translation and tumorigenesis

MicroRNAs (miRNAs) and heterogeneous nuclear ribonucleoproteins (hnRNPs) are families of sequence-specific, posttranscriptional modulators of gene expression. Despite extensive mechanistic and functional studies on both regulatory classes, the interactions and crosstalk between them are largely unexplored. We have reported that competition between miR-297 and hnRNP L to bind a 3΄UTR-localized C...

متن کامل

MicroRNAs: From Decay to Decoy

MicroRNAs interact with Argonaute proteins to guide posttranscriptional gene silencing. Eiring et al. (2010) now show that miR-328 has a second function, acting as a decoy by binding to hnRNP E2 and lifting its translational repression of an mRNA involved in myeloid cell differentiation.

متن کامل

MicroRNAs Act as Decoy Molecules to Inhibit the Function of RNA Binding Proteins

RNA Binding Proteins Anna M. Eiring *1 Abstract Altered microRNA (miRNA) expression contributes to aberrant post-transcriptional gene regulation in several types of cancers; however, their role in the progression of chronic myeloid leukemia (CML) from chronic phase (CML-CP) to blast crisis (CML-BC) is still largely unknown. To gain further insight into the role of miRNAs in CML disease progress...

متن کامل

افزایش بیان اختصاصی ژن Cdk9 بوسیله microRNA-1 بالغ تک رشته در سلول های فیبروبلاست

Abstract Background: MicroRNAs (miRNAs) are endogenous, non-coding short RNAs (~22 nt) that can downregulate gene expression by translational repression, mRNA degradation, or transcriptional repression. miRNA misregulation has been implicated in pathogenic alterations such as cancer. In order to investigate microRNA functions in gene regulation and/or to modulate their expression in pathogenic...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Cell

دوره 140  شماره 

صفحات  -

تاریخ انتشار 2010