Investigational agent MLN9708/2238 targets tumor-suppressor miR33b in MM cells. Tian, Z., Zhao, J., Tai, Y., Amin, S. B., Hu, Y., Berger, A. J., Richardson, P., Chauhan, D., & Anderson, K. C. Blood, 120(19):3958–3967, November, 2012. ![Investigational agent MLN9708/2238 targets tumor-suppressor miR33b in MM cells. [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex miRs play a critical role in tumor pathogenesis as either oncogenes or tumor-suppressor genes. However, the role of miRs and their regulation in response to proteasome inhibitors in multiple myeloma (MM) is unclear. In the current study, miR profiling in proteasome inhibitor MLN2238-treated MM.1S MM cells shows up-regulation of miR33b. Mechanistic studies indicate that the induction of miR33b is predominantly via transcriptional regulation. Examination of miR33b in patient MM cells showed a constitutively low expression. Overexpression of miR33b decreased MM cell viability, migration, colony formation, and increased apoptosis and sensitivity of MM cells to MLN2238 treatment. In addition, overexpression of miR33b or MLN2238 exposure negatively regulated oncogene PIM-1 and blocked PIM-1 wild-type, but not PIM-1 mutant, luciferase activity. Moreover, PIM-1 overexpression led to significant abrogation of miR33b- or MLN2238-induced cell death. SGI-1776, a biochemical inhibitor of
@article{tian_investigational_2012,
title = {Investigational agent {MLN}9708/2238 targets tumor-suppressor {miR}33b in {MM} cells.},
volume = {120},
url = {http://www.bloodjournal.org/content/120/19/3958},
doi = {10.1182/blood-2012-01-401794},
abstract = {miRs play a critical role in tumor pathogenesis as either oncogenes or tumor-suppressor genes. However, the role of miRs and their regulation in response to proteasome inhibitors in multiple myeloma (MM) is unclear. In the current study, miR profiling in proteasome inhibitor MLN2238-treated MM.1S MM cells shows up-regulation of miR33b. Mechanistic studies indicate that the induction of miR33b is predominantly via transcriptional regulation. Examination of miR33b in patient MM cells showed a constitutively low expression. Overexpression of miR33b decreased MM cell viability, migration, colony formation, and increased apoptosis and sensitivity of MM cells to MLN2238 treatment. In addition, overexpression of miR33b or MLN2238 exposure negatively regulated oncogene PIM-1 and blocked PIM-1 wild-type, but not PIM-1 mutant, luciferase activity. Moreover, PIM-1 overexpression led to significant abrogation of miR33b- or MLN2238-induced cell death. SGI-1776, a biochemical inhibitor of},
language = {eng},
number = {19},
journal = {Blood},
author = {Tian, Ze and Zhao, Jian-jun and Tai, Yu-Tzu and Amin, Samir B. and Hu, Yiguo and Berger, Allison J. and Richardson, Paul and Chauhan, Dharminder and Anderson, Kenneth C.},
month = nov,
year = {2012},
pmid = {22983447},
pmcid = {PMC3496955},
keywords = {microrna, multiple\_myeloma},
pages = {3958--3967},
authorclass = {coauthor},
contribution = {data\_analysis, interpretation},
affiliation = {DFCI}
}
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