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HDAC inhibitor Vorinostat and BET inhibitor Plx51107 epigenetic agents' combined treatments exert a therapeutic approach upon acute myeloid leukemia cell model. | LitMetric

AI Article Synopsis

  • The development of cancer involves changes in gene expression driven by genomic and epigenetic factors.
  • This study explored the effects of a new BRD inhibitor, PLX51107, and the HDAC inhibitor Vorinostat (SAHA) on cell behaviors such as proliferation, apoptosis, and gene regulation in both leukemia cells (HL60) and healthy B-lymphocytes (NCIBL2171).
  • Results showed that using PLX51107 and Vorinostat together enhanced the treatment's effectiveness, promoting cell death and halting cell growth more effectively than either drug alone, indicating potential for clinical application in treating blood cancers.

Article Abstract

The process of cancer initiation and development is regulated via the transcriptional expression of cells going under genomic and epigenetic changes. Targeting epigenetic "readers", i.e., bromodomains (BRD) and post-translational modifications of nucleosomal histone proteins regulate gene expression in both cancerous and healthy cells. In this study, the new epigenetic agent BRD inhibitor PLX51107 and histone deacetylase (HDAC) inhibitor SAHA' s (Vorinostat) single/combined applications' reflections were analyzed in case of cell proliferation, cytotoxicity, apoptosis, cell cycle arrest, and finally target gene expression regulation upon both AML and healthy B-lymphocyte cells; HL60 and NCIBL2171, respectively; in vitro. Since mono treatments of either Vorinostat or Plx51107 regulated cellular responses such as growth, proliferation, apoptosis, and cell cycle arrest of tumor cells; their combination treatments exerted accelerated results. We detected that combined treatment of Plx51107 and Vorinostat strengthened effects detected upon leukemic cells for gaining more sensitization to the agents, decreasing cell proliferation, dramatically inducing apoptosis, and cell cycle arrest; thus regulating target gene expressions. We have shown for the first time that the newly analyzed BRD inhibitor Plx51107 could be a promising therapeutic approach for hematological malignancies and its mono or combined usage might support a rapid transition to clinical trials.

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Source
http://dx.doi.org/10.1007/s12032-022-01858-xDOI Listing

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