Abstract
Nuclear-cytoplasmic shuttling is a highly regulated and complex process, which involves both proteins and nucleic acids. Changes in cellular compartmentalization of various proteins, including oncogenes and tumor suppressors, affect cellular behavior, promoting or inhibiting proliferation, apoptosis and sensitivity to therapies. In this review, we will recapitulate the role of various shuttling components in Chronic Myeloid Leukemia and we will provide insights on the potential role of shuttling proteins as therapeutic targets.
Highlights
Shuttling from the nucleus to the cytoplasm and back is a highly regulated and complex process, which may include proteins and nucleic acids such as mRNA molecules [1,2,3]
All together these data clearly point to the issue that the leading oncogene of Chronic Myeloid Leukemia (CML) may turn into a suicide gene, when delocalized, and that shifting cellular compartments is achievable with the combination of various drugs
Not surprisingly, altered expression of some RNA-binding proteins (RBP) with nuclear-cytoplasmic shuttling activity has been shown in BCR/ABL leukemogenesis [54]
Summary
Shuttling from the nucleus to the cytoplasm and back is a highly regulated and complex process, which may include proteins and nucleic acids such as mRNA molecules [1,2,3]. The identification of shuttling tumor suppressors and the mechanisms that promote their delocalization in the cell may allow the development of therapies to restore the proper cellular compartmentalization with consequent re-activation of the tumor suppressive functions [8]. All together these data clearly point to the issue that the leading oncogene of CML may turn into a suicide gene, when delocalized, and that shifting cellular compartments is achievable with the combination of various drugs.
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