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ALK-mediated post-transcriptional regulation: focus on RNA-binding proteins

Julie Bergalet, Mohamad Fawal, Dominique Morello

  • 1Centre de Recherche en Cancerologie de Toulouse (CRCT), UMR 1037, INSERM-UPS, ERL5294 CNRS, 2 avenue Hubert Curien, Oncopole entree C, CS 53717, 31037 Toulouse Cedex 1, France, estelle.espinos@inserm.fr.

Frontiers in Bioscience (Landmark Edition)
|May 12, 2015
PubMed

Insights

Nucleophosmin-Anaplastic Lymphoma Kinase (NPM-ALK) oncogenic effects involve post-transcriptional regulation by RNA-binding proteins (RBPs). This review explores NPM-ALK

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The oncogenic Nucleophosmin-Anaplastic Lymphoma Kinase (NPM-ALK) has been extensively studied for its role in cancer.
  • NPM-ALK's known mechanisms involve transcriptional regulation via signaling pathways like JAK3/STAT3, PI3K/AKT, and RAS/ERK.
  • Recent discoveries highlight potential post-transcriptional roles involving RNA-binding proteins (RBPs) interacting with ALK.

Purpose of the Study:

  • To review emerging insights into NPM-ALK-mediated post-transcriptional regulation.
  • To focus on the association between NPM-ALK and specific RBPs.
  • To discuss the function of ALK granules (AGs) in anaplastic large cell lymphoma (ALCL).

Main Methods:

  • Literature review of studies on NPM-ALK and its interactome.
  • Analysis of the role of RBPs in NPM-ALK's oncogenic activity.
  • Examination of the composition and nature of ALK granules (AGs).

Main Results:

  • NPM-ALK modulates the biological properties of associated RBPs.
  • Cytoplasmic aggregates, termed ALK granules (AGs), are observed in ALK-positive ALCL.
  • AGs contain polyadenylated mRNAs and RBPs, distinct from PBs and SGs.

Conclusions:

  • NPM-ALK exerts oncogenic effects through both transcriptional and post-transcriptional mechanisms.
  • RBPs play a significant role in NPM-ALK's function at the post-transcriptional level.
  • ALK granules represent a novel cellular compartment involved in mRNA fate regulation in ALCL.

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