Akt-mediated Ephexin1-Ras interaction promotes oncogenic Ras signaling and colorectal and lung cancer cell proliferation.


Journal

Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092

Informations de publication

Date de publication:
28 10 2021
Historique:
received: 20 08 2021
accepted: 13 10 2021
revised: 12 10 2021
entrez: 29 10 2021
pubmed: 30 10 2021
medline: 3 2 2022
Statut: epublish

Résumé

Ephexin1 was reported to be highly upregulated by oncogenic Ras, but the functional consequences of this remain poorly understood. Here, we show that Ephexin1 is highly expressed in colorectal cancer (CRC) and lung cancer (LC) patient tissues. Knockdown of Ephexin1 markedly inhibited the cell growth of CRC and LC cells with oncogenic Ras mutations. Ephexin1 contributes to the positive regulation of Ras-mediated downstream target genes and promotes Ras-induced skin tumorigenesis. Mechanically, Akt phosphorylates Ephexin1 at Ser16 and Ser18 (pSer16/18) and pSer16/18 Ephexin1 then interacts with oncogenic K-Ras to promote downstream MAPK signaling, facilitating tumorigenesis. Furthermore, pSer16/18 Ephexin1 is associated with both an increased tumor grade and metastatic cases of CRC and LC, and those that highly express pSer16/18 exhibit poor overall survival rates. These data indicate that Ephexin1 plays a critical role in the Ras-mediated CRC and LC and pSer16/18 Ephexin1 might be an effective therapeutic target for CRC and LC.

Identifiants

pubmed: 34711817
doi: 10.1038/s41419-021-04332-0
pii: 10.1038/s41419-021-04332-0
pmc: PMC8553951
doi:

Substances chimiques

Guanine Nucleotide Exchange Factors 0
NGEF protein, human 0
RNA, Messenger 0
Phosphoserine 17885-08-4
Proto-Oncogene Proteins c-akt EC 2.7.11.1
ras Proteins EC 3.6.5.2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1013

Subventions

Organisme : National Research Foundation of Korea (NRF)
ID : 2019R1A6A3A01092483
Organisme : National Research Foundation of Korea (NRF)
ID : 2015R1A5A2009070
Organisme : National Research Foundation of Korea (NRF)
ID : 2021R1A2C2005652

Informations de copyright

© 2021. The Author(s).

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Auteurs

Jeeho Kim (J)

Laboratory of Genomic Instability and Cancer therapeutics, Chosun University School of medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea.
Department of Pharmacology, Chosun University School of medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea.

Young Jin Jeon (YJ)

Department of Pharmacology, Chosun University School of medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea.

Sung-Chul Lim (SC)

Department of Pathology, Chosun University School of medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea.

Joohyun Ryu (J)

The Hormel Institute, University of Minnesota, 801 16th Avenue NE, Austin, MN, 55912, USA.

Jung-Hee Lee (JH)

Laboratory of Genomic Instability and Cancer therapeutics, Chosun University School of medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea.
Department of Cellular and Molecular Medicine, Chosun University School of medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea.

In-Youb Chang (IY)

Department of Anatomy, Chosun University School of medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea. iyjang@chosun.ac.kr.

Ho Jin You (HJ)

Laboratory of Genomic Instability and Cancer therapeutics, Chosun University School of medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea. hjyou@chosun.ac.kr.
Department of Pharmacology, Chosun University School of medicine, 375 Seosuk-Dong, Gwangju, 501-759, South Korea. hjyou@chosun.ac.kr.

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Classifications MeSH