Combination treatment with 2-methoxyestradiol overcomes bortezomib resistance of multiple myeloma cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-10

AUTHORS

In-Sung Song, Yu Jeong Jeong, Seung Hun Jeong, Hye Jin Heo, Hyoung Kyu Kim, Sung Ryul Lee, Tae Hee Ko, Jae Boum Youm, Nari Kim, Kyung Soo Ko, Byoung Doo Rhee, Jin Han

ABSTRACT

Bortezomib is a proteasome inhibitor used for the treatment of relapsed/refractory multiple myeloma (MM). However, intrinsic and acquired resistance to bortezomib has already been observed in MM patients. In a previous report, we demonstrated that changes in the expression of mitochondrial genes lead to changes in mitochondrial activity and bortezomib susceptibility or resistance, and their combined effects contribute to the differential sensitivity or resistance of MM cells to bortezomib. Here we report that the combination treatment of bortezomib and 2-methoxyestradiol (2ME), a natural estrogen metabolite, induces mitochondria-mediated apoptotic cell death of bortezomib-resistant MM KMS20 cells via mitochondrial reactive oxygen species (ROS) overproduction. Bortezomib plus 2ME treatment induces a higher level of cell death compared with treatment with bortezomib alone and increases mitochondrial ROS and Ca(2+) levels in KMS20 cells. Pretreatment with the antioxidant N-acetyl-L-cysteine scavenges mitochondrial ROS and decreases cell death after treatment with bortezomib plus 2ME in KMS20 cells. Moreover, we observed that treatment with bortezomib plus 2ME maintains the activation of c-Jun N-terminal kinase (JNK) and mitogen-activated protein kinase kinase kinase 4/7 (MKK4/7). Collectively, combination treatment with bortezomib and 2ME induces cell death via JNK-MKK4/7 activation by overproduction of mitochondrial ROS. Therefore, combination therapy with specific mitochondrial-targeting drugs may prove useful to the development of novel strategies for the treatment of bortezomib-resistant MM patients. More... »

PAGES

emm2013104

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/emm.2013.104

DOI

http://dx.doi.org/10.1038/emm.2013.104

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1007121240

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24158003


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