STK38 is a critical upstream regulator of MYC's oncogenic activity in human B-cell lymphoma

The MYC protooncogene is associated with the pathogenesis of most human neoplasia. Conversely, its experimental inactivation elicits oncogene addiction. Besides constituting a formidable therapeutic target, MYC also has an essential function in normal physiology, thus creating the need for context-s...

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Published inOncogene Vol. 32; no. 45; pp. 5283 - 5291
Main Authors Bisikirska, B C, Adam, S J, Alvarez, M J, Rajbhandari, P, Cox, R, Lefebvre, C, Wang, K, Rieckhof, G E, Felsher, D W, Califano, A
Format Journal Article
LanguageEnglish
Published England Nature Publishing Group 07.11.2013
Subjects
Animals
Apoptosis
B-Lymphocytes - metabolism
Carcinogenesis
Cell Line, Tumor
Cell Transformation, Neoplastic - genetics
Cells
Gene Expression Regulation, Neoplastic
Genes
Genetic aspects
HEK293 Cells
HeLa Cells
Heterografts
Humans
Lymphoma
Lymphoma, B-Cell - metabolism
Mice
Mice, SCID
Neoplasm Transplantation
Phosphotransferases
Properties
Protein Processing, Post-Translational
Protein-protein interactions
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - metabolism
Proteins
Proto-Oncogene Proteins c-myc - metabolism
Receptors, Antigen, B-Cell - metabolism
RNA Interference
RNA, Small Interfering
Testing
Tumors
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Abstract The MYC protooncogene is associated with the pathogenesis of most human neoplasia. Conversely, its experimental inactivation elicits oncogene addiction. Besides constituting a formidable therapeutic target, MYC also has an essential function in normal physiology, thus creating the need for context-specific targeting strategies. The analysis of post-translational MYC activity modulation yields novel targets for MYC inactivation. Specifically, following regulatory network analysis in human B-cells, we identify a novel role of the STK38 kinase as a regulator of MYC activity and a candidate target for abrogating tumorigenesis in MYC-addicted lymphoma. We found that STK38 regulates MYC protein stability and turnover in a kinase activity-dependent manner. STK38 kinase inactivation abrogates apoptosis following B-cell receptor activation, whereas its silencing significantly decreases MYC levels and increases apoptosis. Moreover, STK38 knockdown suppresses growth of MYC-addicted tumors in vivo, thus providing a novel viable target for treating these malignancies.
AbstractList The MYC protooncogene is associated with the pathogenesis of most human neoplasia. Conversely, its experimental inactivation elicits oncogene addiction. Besides constituting a formidable therapeutic target, MYC also has an essential function in normal physiology, thus creating the need for context-specific targeting strategies. The analysis of post-translational MYC activity modulation yields novel targets for MYC inactivation. Specifically, following regulatory network analysis in human B-cells, we identify a novel role of the STK38 kinase as a regulator of MYC activity and a candidate target for abrogating tumorigenesis in MYC-addicted lymphoma. We found that STK38 regulates MYC protein stability and turnover in a kinase activity-dependent manner. STK38 kinase inactivation abrogates apoptosis following B-cell receptor activation, whereas its silencing significantly decreases MYC levels and increases apoptosis. Moreover, STK38 knockdown suppresses growth of MYC-addicted tumors in vivo, thus providing a novel viable target for treating these malignancies. Oncogene (2013) 32, 5283-5291; doi: 10.1038/onc.2012.543; published online 26 November 2012 Keywords: STK38; MYC post-translational modifications; protein turnover; transcriptional activity; protein-protein interaction
The MYC protooncogene is associated with the pathogenesis of most human neoplasia. Conversely, its experimental inactivation elicits oncogene addiction. Besides constituting a formidable therapeutic target, MYC also has an essential function in normal physiology, thus creating the need for context-specific targeting strategies. The analysis of post-translational MYC activity modulation yields novel targets for MYC inactivation. Specifically, following regulatory network analysis in human B-cells, we identify a novel role of the STK38 kinase as a regulator of MYC activity and a candidate target for abrogating tumorigenesis in MYC-addicted lymphoma. We found that STK38 regulates MYC protein stability and turnover in a kinase activity-dependent manner. STK38 kinase inactivation abrogates apoptosis following B-cell receptor activation, whereas its silencing significantly decreases MYC levels and increases apoptosis. Moreover, STK38 knockdown suppresses growth of MYC-addicted tumors in vivo, thus providing a novel viable target for treating these malignancies.
The MYC proto-oncogene is associated with the pathogenesis of most human neoplasia. Conversely, its experimental inactivation elicits oncogene addiction. While MYC constitutes a formidable therapeutic target, it also plays an essential role in normal physiology, thus creating the need for context--specific targeting strategies. The analysis of post-translational MYC activity modulation yields novel targets for MYC inactivation. Specifically, following regulatory network analysis in human B cells, we identify a novel role of the STK38 kinase as a regulator of MYC activity and a candidate target for abrogating tumorigenesis in MYC addicted lymphoma. We found that STK38 regulates MYC protein stability and turnover in a kinase-activity-dependent manner. STK38 kinase inactivation abrogates apoptosis following B-cell receptor (BCR) activation, while its silencing significantly decreases MYC levels and increases apoptosis. Moreover, STK38 knockdown suppresses growth of MYC addicted tumors in vivo thus providing a novel viable target for treating these malignancies.
Audience Academic
Author Felsher, D W
Adam, S J
Wang, K
Alvarez, M J
Rajbhandari, P
Rieckhof, G E
Cox, R
Bisikirska, B C
Lefebvre, C
Califano, A
AuthorAffiliation 4 Department of Biomedical Informatics, Columbia University, New York, New York
6 Bronx, New York; Pfizer, Inc. San Diego, California
3 Department of Pathology and Genetics & Development, Columbia University, New York, New York
1 Joint Centers for Systems Biology, Columbia University, New York, New York
2 Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, California
5 Riverdale Country School, San Diego, California
AuthorAffiliation_xml – name: 5 Riverdale Country School, San Diego, California
– name: 4 Department of Biomedical Informatics, Columbia University, New York, New York
– name: 6 Bronx, New York; Pfizer, Inc. San Diego, California
– name: 3 Department of Pathology and Genetics & Development, Columbia University, New York, New York
– name: 1 Joint Centers for Systems Biology, Columbia University, New York, New York
– name: 2 Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, California
Author_xml – sequence: 1
  givenname: B C
  surname: Bisikirska
  fullname: Bisikirska, B C
  organization: Joint Centers for Systems Biology, Columbia University, New York, NY, USA
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/23178486$$D View this record in MEDLINE/PubMed
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SSID ssj0007902
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Snippet The MYC protooncogene is associated with the pathogenesis of most human neoplasia. Conversely, its experimental inactivation elicits oncogene addiction....
The MYC proto-oncogene is associated with the pathogenesis of most human neoplasia. Conversely, its experimental inactivation elicits oncogene addiction. While...
SourceID pubmedcentral
proquest
gale
crossref
pubmed
SourceType Open Access Repository
Aggregation Database
Index Database
StartPage 5283
SubjectTerms Animals
Apoptosis
B-Lymphocytes - metabolism
Carcinogenesis
Cell Line, Tumor
Cell Transformation, Neoplastic - genetics
Cells
Gene Expression Regulation, Neoplastic
Genes
Genetic aspects
HEK293 Cells
HeLa Cells
Heterografts
Humans
Lymphoma
Lymphoma, B-Cell - metabolism
Mice
Mice, SCID
Neoplasm Transplantation
Phosphotransferases
Properties
Protein Processing, Post-Translational
Protein-protein interactions
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - metabolism
Proteins
Proto-Oncogene Proteins c-myc - metabolism
Receptors, Antigen, B-Cell - metabolism
RNA Interference
RNA, Small Interfering
Testing
Tumors
Title STK38 is a critical upstream regulator of MYC's oncogenic activity in human B-cell lymphoma
URI https://www.ncbi.nlm.nih.gov/pubmed/23178486
https://www.proquest.com/docview/1449100744/abstract/
https://search.proquest.com/docview/1464513562
https://pubmed.ncbi.nlm.nih.gov/PMC3715597
Volume 32
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