Extracellular signal-regulated kinases associate with and phosphorylate DHPS to promote cell proliferation.


Journal

Oncogenesis
ISSN: 2157-9024
Titre abrégé: Oncogenesis
Pays: United States
ID NLM: 101580004

Informations de publication

Date de publication:
28 Sep 2020
Historique:
received: 27 05 2020
accepted: 15 09 2020
revised: 30 08 2020
entrez: 29 9 2020
pubmed: 30 9 2020
medline: 30 9 2020
Statut: epublish

Résumé

The ERK1/2 pathway is one of the most commonly dysregulated pathways in human cancers and controls many vital cellular processes. Although many ERK1/2 kinase substrates have been identified, the diversity of ERK1/2 mediated processes suggests the existence of additional targets. Here, we identified Deoxyhypusine synthase (DHPS), an essential hypusination enzyme regulating protein translation, as a major and direct-binding protein of ERK1/2. Further experiments showed that ERK1/2 phosphorylate DHPS at Ser-233 site. The Ser-233 phosphorylation of DHPS by ERK1/2 is important for its function in cell proliferation. Moreover, we found that higher DHPS expression correlated with poor prognosis in lung adenocarcinoma and increased resistance to inhibitors of the ERK1/2 pathway. In summary, our results suggest that ERK1/2-mediated DHPS phosphorylation is an important mechanism that underlies protein translation and that DHPS expression is a potent biomarker of response to therapies targeting ERK1/2-pathway.

Identifiants

pubmed: 32989218
doi: 10.1038/s41389-020-00271-1
pii: 10.1038/s41389-020-00271-1
pmc: PMC7522278
doi:

Types de publication

Journal Article

Langues

eng

Pagination

85

Subventions

Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : CA210929
Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : CA193124
Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : CA216437
Organisme : U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)
ID : CA216911
Organisme : Cancer Prevention and Research Institute of Texas (Cancer Prevention Research Institute of Texas)
ID : RP160667
Organisme : NCI NIH HHS
ID : R01 CA216437
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA216911
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA016672
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA210929
Pays : United States

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Auteurs

Chao Wang (C)

Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.

Zhen Chen (Z)

Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.

Litong Nie (L)

Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.

Mengfan Tang (M)

Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.

Xu Feng (X)

Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.

Dan Su (D)

Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.

Huimin Zhang (H)

Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.

Yun Xiong (Y)

Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.

Jeong-Min Park (JM)

Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.

Junjie Chen (J)

Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA. jchen8@mdanderson.org.

Classifications MeSH