Tilting MYC toward cancer cell death.

Autor: Harrington CT; Division of Cancer Pathobiology, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA; Cell and Molecular Biology Graduate Group, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA., Sotillo E; Division of Cancer Pathobiology, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA., Dang CV; Cell and Molecular Biology Graduate Group, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA; Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, PA 19104, USA; Ludwig Institute for Cancer Research, New York, NY 10017, USA., Thomas-Tikhonenko A; Division of Cancer Pathobiology, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA; Cell and Molecular Biology Graduate Group, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: andreit@pennmedicine.upenn.edu.
Jazyk: angličtina
Zdroj: Trends in cancer [Trends Cancer] 2021 Nov; Vol. 7 (11), pp. 982-994. Date of Electronic Publication: 2021 Sep 02.
DOI: 10.1016/j.trecan.2021.08.002
Abstrakt: MYC oncoprotein promotes cell proliferation and serves as the key driver in many human cancers; therefore, considerable effort has been expended to develop reliable pharmacological methods to suppress its expression or function. Despite impressive progress, MYC-targeting drugs have not reached the clinic. Recent advances suggest that within a limited expression range unique to each tumor, MYC oncoprotein can have a paradoxical, proapoptotic function. Here we introduce a counterintuitive idea that modestly and transiently elevating MYC levels could aid chemotherapy-induced apoptosis and thus benefit the patients as much, if not more than MYC inhibition.
Competing Interests: Declaration of interests A.T-T. and E.S. are inventors on the US Patent US10751356B2 ‘Compositions and methods for transient upregulation of MYC in B-cell lymphomas for enhancing P53 independent apoptotic responses to chemotherapy’. This intellectual property is held by CHOP and to date has not been licensed or otherwise commercialized. A.T-T. receives funding from Pfizer’s ASPIRE Program for research unrelated to the topic of this review.
(Copyright © 2021 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE