The crucial p53-dependent oncogenic role of JAB1 in osteosarcoma in vivo.


Journal

Oncogene
ISSN: 1476-5594
Titre abrégé: Oncogene
Pays: England
ID NLM: 8711562

Informations de publication

Date de publication:
06 2020
Historique:
received: 20 08 2019
accepted: 28 04 2020
revised: 23 04 2020
pubmed: 12 5 2020
medline: 26 11 2020
entrez: 12 5 2020
Statut: ppublish

Résumé

Osteosarcoma (OS) is the most common primary bone cancer and ranks amongst the leading causes of cancer mortality in young adults. Jun activation domain-binding protein 1 (JAB1) is overexpressed in many cancers and has recently emerged as a novel target for cancer treatment. However, the role of JAB1 in osteosarcoma was virtually unknown. In this study, we demonstrate that JAB1-knockdown in malignant osteosarcoma cell lines significantly reduced their oncogenic properties, including proliferation, colony formation, and motility. We also performed RNA-sequencing analysis in JAB1-knockdown OS cells and identified 4110 genes that are significantly differentially expressed. This demonstrated for the first time that JAB1 regulates a large and specific transcriptome in cancer. We also found that JAB1 is overexpressed in human OS and correlates with a poor prognosis. Moreover, we generated a novel mouse model that overexpresses Jab1 specifically in osteoblasts upon a TP53 heterozygous sensitizing background. Interestingly, by 13 months of age, a significant proportion of these mice spontaneously developed conventional OS. Finally, we demonstrate that a novel, highly specific small molecule inhibitor of JAB1, CSN5i-3, reduces osteosarcoma cell viability, and has specific effects on the ubiquitin-proteasome system in OS. Thus, we show for the first time that the overexpression of JAB1 in vivo can result in accelerated spontaneous tumor formation in a p53-dependent manner. In summary, JAB1 might be a unique target for the treatment of osteosarcoma and other cancers.

Identifiants

pubmed: 32390003
doi: 10.1038/s41388-020-1320-6
pii: 10.1038/s41388-020-1320-6
pmc: PMC7274902
mid: NIHMS1589186
doi:

Substances chimiques

Intracellular Signaling Peptides and Proteins 0
TP53 protein, human 0
Tumor Suppressor Protein p53 0
Peptide Hydrolases EC 3.4.-
COPS5 protein, human EC 3.4.-.-
COP9 Signalosome Complex EC 3.4.19.12

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4581-4591

Subventions

Organisme : NIAMS NIH HHS
ID : R01 AR068361
Pays : United States
Organisme : NCI NIH HHS
ID : R03 CA175874
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA043703
Pays : United States
Organisme : NIAMS NIH HHS
ID : T32 AR007505
Pays : United States

Références

Mirabello L, Troisi RJ, Savage SA. Osteosarcoma incidence and survival rates from 1973 to 2004: data from the surveillance, epidemiology, and end results program. Cancer. 2009;115:1531–43.
pubmed: 19197972 pmcid: 2813207
Gianferante DM, Mirabello L, Savage SA. Germline and somatic genetics of osteosarcoma—connecting aetiology, biology and therapy. Nat Rev Endocrinol. 2017;13:480–91.
pubmed: 28338660
Donehower LA, Harvey M, Slagle BL, McArthur MJ, Montgomery CA Jr., Butel JS, et al. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours. Nature. 1992;356:215–21.
pubmed: 1552940
Jacks T, Remington L, Williams BO, Schmitt EM, Halachmi S, Bronson RT, et al. Tumor spectrum analysis in p53-mutant mice. Curr Biol. 1994;4:1–7.
pubmed: 7922305
Lin PP, Pandey MK, Jin F, Raymond AK, Akiyama H, Lozano G. Targeted mutation of p53 and Rb in mesenchymal cells of the limb bud produces sarcomas in mice. Carcinogenesis. 2009;30:1789–95.
pubmed: 19635748 pmcid: 4141195
Walkley CR, Qudsi R, Sankaran VG, Perry JA, Gostissa M, Roth SI, et al. Conditional mouse osteosarcoma, dependent on p53 loss and potentiated by loss of Rb, mimics the human disease. Genes Dev. 2008;22:1662–76.
pubmed: 18559481 pmcid: 2428063
Berman SD, Calo E, Landman AS, Danielian PS, Miller ES, West JC, et al. Metastatic osteosarcoma induced by inactivation of Rb and p53 in the osteoblast lineage. Proc Natl Acad Sci USA. 2008;105:11851–6.
pubmed: 18697945
Kato JY, Yoneda-Kato N. Mammalian COP9 signalosome. Genes Cells. 2009;14:1209–25.
pubmed: 19849719
Liu G, Claret FX, Zhou F, Pan Y. Jab1/COPS5 as a novel biomarker for diagnosis, prognosis, therapy prediction and therapeutic tools for human cancer. Front Pharmacol. 2018;9:135.
pubmed: 29535627 pmcid: 5835092
Wei N, Serino G, Deng XW. The COP9 signalosome: more than a protease. Trends Biochem Sci. 2008;33:592–600.
pubmed: 18926707
Claret FX, Hibi M, Dhut S, Toda T, Karin M. A new group of conserved coactivators that increase the specificity of AP-1 transcription factors. Nature. 1996;383:453–7.
pubmed: 8837781
Bashur LA, Chen D, Chen Z, Liang B, Pardi R, Murakami S, et al. Loss of jab1 in osteochondral progenitor cells severely impairs embryonic limb development in mice. J Cell Physiol. 2014;229:1607–17.
pubmed: 24604556 pmcid: 4157318
Chen D, Bashur LA, Liang B, Panattoni M, Tamai K, Pardi R, et al. The transcriptional co-regulator Jab1 is crucial for chondrocyte differentiation in vivo. J Cell Sci. 2013;126:234–43.
pubmed: 23203803 pmcid: 3603518
Sitte S, Glasner J, Jellusova J, Weisel F, Panattoni M, Pardi R, et al. JAB1 is essential for B cell development and germinal center formation and inversely regulates Fas ligand and Bcl6 expression. J Immunol. 2012;188:2677–86.
pubmed: 22327073
Panattoni M, Sanvito F, Basso V, Doglioni C, Casorati G, Montini E, et al. Targeted inactivation of the COP9 signalosome impairs multiple stages of T cell development. J Exp Med. 2008;205:465–77.
pubmed: 18268034 pmcid: 2271025
Oh W, Lee EW, Sung YH, Yang MR, Ghim J, Lee HW, et al. Jab1 induces the cytoplasmic localization and degradation of p53 in coordination with Hdm2. J Biol Chem. 2006;281:17457–65.
pubmed: 16624822
Lauvrak SU, Munthe E, Kresse SH, Stratford EW, Namlos HM, Meza-Zepeda LA, et al. Functional characterisation of osteosarcoma cell lines and identification of mRNAs and miRNAs associated with aggressive cancer phenotypes. Br J Cancer. 2013;109:2228–36.
pubmed: 24064976 pmcid: 3798956
Collier CD, Wirtz EC, Knafler GJ, Morris WZ, Getty PJ, Greenfield EM. Micrometastatic drug screening platform shows heterogeneous response to MAP chemotherapy in osteosarcoma cell lines. Clin Orthop Relat Res. 2018;476:1400–11.
pubmed: 29481344 pmcid: 6437591
Ottaviano L, Schaefer KL, Gajewski M, Huckenbeck W, Baldus S, Rogel U, et al. Molecular characterization of commonly used cell lines for bone tumor research: a trans-European EuroBoNet effort. Genes Chromosomes Cancer. 2010;49:40–51.
pubmed: 19787792
Behjati S, Tarpey PS, Haase K, Ye H, Young MD, Alexandrov LB, et al. Recurrent mutation of IGF signalling genes and distinct patterns of genomic rearrangement in osteosarcoma. Nat Commun. 2017;8:15936.
pubmed: 28643781 pmcid: 5490007
Perry JA, Kiezun A, Tonzi P, Van Allen EM, Carter SL, Baca SC, et al. Complementary genomic approaches highlight the PI3K/mTOR pathway as a common vulnerability in osteosarcoma. Proc Natl Acad Sci USA. 2014;111:E5564–73.
pubmed: 25512523
Zhang F, Yan T, Guo W, Sun K, Wang S, Bao X, et al. Novel oncogene COPS3 interacts with Beclin1 and Raf-1 to regulate metastasis of osteosarcoma through autophagy. J Exp Clin Cancer Res. 2018;37:135.
pubmed: 29970115 pmcid: 6029018
Crone SG, Jacobsen A, Federspiel B, Bardram L, Krogh A, Lund AH, et al. microRNA-146a inhibits G protein-coupled receptor-mediated activation of NF-kappaB by targeting CARD10 and COPS8 in gastric cancer. Mol Cancer. 2012;11:71.
pubmed: 22992343 pmcid: 3515505
Lee YH, Judge AD, Seo D, Kitade M, Gomez-Quiroz LE, Ishikawa T, et al. Molecular targeting of CSN5 in human hepatocellular carcinoma: a mechanism of therapeutic response. Oncogene. 2011;30:4175–84.
pubmed: 21499307 pmcid: 3140552
Huang da W, Sherman BT, Lempicki RA. Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources. Nat Protoc. 2009;4:44–57.
pubmed: 19131956
Huang da W, Sherman BT, Lempicki RA. Bioinformatics enrichment tools: paths toward the comprehensive functional analysis of large gene lists. Nucleic Acids Res. 2009;37:1–13.
pubmed: 19033363
Ballatori SE, Hinds PW. Osteosarcoma: prognosis plateau warrants retinoblastoma pathway targeted therapy. Signal Transduct Target Ther. 2016;1:16001.
pubmed: 29263893 pmcid: 5657420
Loukil A, Cheung CT, Bendris N, Lemmers B, Peter M, Blanchard JM. Cyclin A2: at the crossroads of cell cycle and cell invasion. World J Biol Chem. 2015;6:346–50.
pubmed: 26629317 pmcid: 4657123
Gavet O, Pines J. Progressive activation of CyclinB1-Cdk1 coordinates entry to mitosis. Dev Cell. 2010;18:533–43.
pubmed: 20412769 pmcid: 3325599
Zhou G, Zheng Q, Engin F, Munivez E, Chen Y, Sebald E, et al. Dominance of SOX9 function over RUNX2 during skeletogenesis. Proc Natl Acad Sci USA. 2006;103:19004–9.
pubmed: 17142326
Tao J, Jiang MM, Jiang L, Salvo JS, Zeng HC, Dawson B, et al. Notch activation as a driver of osteogenic sarcoma. Cancer Cell. 2014;26:390–401.
pubmed: 25203324 pmcid: 4159617
Enchev RI, Schulman BA, Peter M. Protein neddylation: beyond cullin-RING ligases. Nat Rev Mol Cell Biol. 2015;16:30–44.
pubmed: 25531226 pmcid: 5131867
Malhab LJ, Descamps S, Delaval B, Xirodimas DP. The use of the NEDD8 inhibitor MLN4924 (Pevonedistat) in a cyclotherapy approach to protect wild-type p53 cells from MLN4924 induced toxicity. Sci Rep. 2016;6:37775.
pubmed: 27901050 pmcid: 5129021
Soucy TA, Smith PG, Milhollen MA, Berger AJ, Gavin JM, Adhikari S, et al. An inhibitor of NEDD8-activating enzyme as a new approach to treat cancer. Nature. 2009;458:732–6.
pubmed: 19360080
Zhou L, Jiang Y, Luo Q, Li L, Jia L. Neddylation: a novel modulator of the tumor microenvironment. Mol Cancer. 2019;18:77.
pubmed: 30943988 pmcid: 6446326
Schlierf A, Altmann E, Quancard J, Jefferson AB, Assenberg R, Renatus M, et al. Targeted inhibition of the COP9 signalosome for treatment of cancer. Nat Commun. 2016;7:13166.
pubmed: 27774986 pmcid: 5078989
Wang Z, Liu P, Inuzuka H, Wei W. Roles of F-box proteins in cancer. Nat Rev Cancer. 2014;14:233–47.
pubmed: 24658274 pmcid: 4306233
Tian L, Peng G, Parant JM, Leventaki V, Drakos E, Zhang Q, et al. Essential roles of Jab1 in cell survival, spontaneous DNA damage and DNA repair. Oncogene. 2010;29:6125–37.
pubmed: 20802511 pmcid: 3495558
Mori M, Yoneda-Kato N, Yoshida A, Kato JY. Stable form of JAB1 enhances proliferation and maintenance of hematopoietic progenitors. J Biol Chem. 2008;283:29011–21.
pubmed: 18667426 pmcid: 2662005
Swords RT, Watts J, Erba HP, Altman JK, Maris M, Anwer F, et al. Expanded safety analysis of pevonedistat, a first-in-class NEDD8-activating enzyme inhibitor, in patients with acute myeloid leukemia and myelodysplastic syndromes. Blood. Cancer J. 2017;7:e520.
Manasanch EE, Orlowski RZ. Proteasome inhibitors in cancer therapy. Nat Rev Clin Oncol. 2017;14:417–33.
pubmed: 28117417 pmcid: 5828026
Pan Y, Zhang Q, Atsaves V, Yang H, Claret FX. Suppression of Jab1/CSN5 induces radio- and chemo-sensitivity in nasopharyngeal carcinoma through changes to the DNA damage and repair pathways. Oncogene. 2013;32:2756–66.
pubmed: 22797071
Pan Y, Wang S, Su B, Zhou F, Zhang R, Xu T, et al. Stat3 contributes to cancer progression by regulating Jab1/Csn5 expression. Oncogene. 2017;36:1069–79.
pubmed: 27524414
Zhang Y, Zvi YS, Batko B, Zaphiros N, O’Donnell EF, Wang J, et al. Down-regulation of Skp2 expression inhibits invasion and lung metastasis in osteosarcoma. Sci Rep. 2018;8:14294.
pubmed: 30250282 pmcid: 6155331
Sun R, Xie HY, Qian JX, Huang YN, Yang F, Zhang FL, et al. FBXO22 possesses both protumorigenic and antimetastatic roles in breast cancer progression. Cancer Res. 2018;78:5274–86.
pubmed: 29945959
Johmura Y, Maeda I, Suzuki N, Wu W, Goda A, Morita M, et al. Fbxo22-mediated KDM4B degradation determines selective estrogen receptor modulator activity in breast cancer. J Clin Investig. 2018;128:5603–19.
pubmed: 30418174
Lu R, Hu X, Zhou J, Sun J, Zhu AZ, Xu X, et al. COPS5 amplification and overexpression confers tamoxifen-resistance in ERalpha-positive breast cancer by degradation of NCoR. Nat Commun. 2016;7:12044.
pubmed: 27375289 pmcid: 4932188
Liang B, Cotter MM, Chen D, Hernandez CJ, Zhou G. Ectopic expression of SOX9 in osteoblasts alters bone mechanical properties. Calcif Tissue Int. 2012;90:76–89.
pubmed: 22143895

Auteurs

William E Samsa (WE)

Department of Orthopaedics, Case Western Reserve University, Cleveland, OH, USA.
Case Comprehensive Cancer Center, Cleveland, OH, USA.

Murali K Mamidi (MK)

Department of Orthopaedics, Case Western Reserve University, Cleveland, OH, USA.
Case Comprehensive Cancer Center, Cleveland, OH, USA.

Lindsay A Bashur (LA)

Department of Orthopaedics, Case Western Reserve University, Cleveland, OH, USA.

Robin Elliott (R)

Department of Pathology, Cleveland, OH, USA.

Alexander Miron (A)

Case Comprehensive Cancer Center, Cleveland, OH, USA.
Department of Genetics and Genome Sciences, Cleveland, OH, USA.

Yuqing Chen (Y)

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.

Brendan Lee (B)

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.

Edward M Greenfield (EM)

Indiana University School of Medicine, Indianapolis, IN, USA.

Ricky Chan (R)

Case Comprehensive Cancer Center, Institute for Computational Biology, Cleveland, OH, USA.

David Danielpour (D)

Case Comprehensive Cancer Center, Cleveland, OH, USA.
Division of General Medical Sciences, Cleveland, OH, USA.

Guang Zhou (G)

Department of Orthopaedics, Case Western Reserve University, Cleveland, OH, USA. gxz27@case.edu.
Case Comprehensive Cancer Center, Cleveland, OH, USA. gxz27@case.edu.
Department of Genetics and Genome Sciences, Cleveland, OH, USA. gxz27@case.edu.

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