A peptide derived from adaptor protein STAP-2 inhibits tumor progression by downregulating epidermal growth factor receptor signaling.


Journal

The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R

Informations de publication

Date de publication:
01 2023
Historique:
received: 07 07 2022
revised: 12 11 2022
accepted: 14 11 2022
pubmed: 22 11 2022
medline: 28 1 2023
entrez: 21 11 2022
Statut: ppublish

Résumé

Signal-transducing adaptor family member-2 (STAP-2) is an adaptor protein that regulates various intracellular signals. We previously demonstrated that STAP-2 binds to epidermal growth factor receptor (EGFR) and facilitates its stability and activation of EGFR signaling in prostate cancer cells. Inhibition of this interaction may be a promising direction for cancer treatment. Here, we found that 2D5 peptide, a STAP-2-derived peptide, blocked STAP-2-EGFR interactions and suppressed EGFR-mediated proliferation in several cancer cell lines. 2D5 peptide inhibited tumor growth of human prostate cancer cell line DU145 and human lung cancer cell line A549 in murine xenograft models. Additionally, we determined that EGFR signaling and its stability were decreased by 2D5 peptide treatment during EGF stimulation. In conclusion, our study shows that 2D5 peptide is a novel anticancer peptide that inhibits STAP-2-mediated activation of EGFR signaling and suppresses prostate and lung cancer progression.

Identifiants

pubmed: 36410436
pii: S0021-9258(22)01167-X
doi: 10.1016/j.jbc.2022.102724
pmc: PMC9800302
pii:
doi:

Substances chimiques

Adaptor Proteins, Signal Transducing 0
Epidermal Growth Factor 62229-50-9
ErbB Receptors EC 2.7.10.1
STAP2 protein, human 0
Peptides 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

102724

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest All authors declare no conflicts of interest in regard to this article.

Auteurs

Taiga Maemoto (T)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Yuichi Kitai (Y)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan. Electronic address: yu-kitai@pharm.hokudai.ac.jp.

Runa Takahashi (R)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Haruka Shoji (H)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Shunsuke Yamada (S)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Shiho Takei (S)

Faculty of Advanced Life Science, Hokkaido University, Sapporo, Hokkaido, Japan.

Daiki Ito (D)

Faculty of Advanced Life Science, Hokkaido University, Sapporo, Hokkaido, Japan.

Ryuta Muromoto (R)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Jun-Ichi Kashiwakura (JI)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.

Haruka Handa (H)

Department of Molecular Biology, Faculty of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.

Ari Hashimoto (A)

Department of Molecular Biology, Faculty of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.

Shigeru Hashimoto (S)

Division of Molecular Psychoimmunology, Graduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.

Toyoyuki Ose (T)

Faculty of Advanced Life Science, Hokkaido University, Sapporo, Hokkaido, Japan.

Kenji Oritani (K)

Department of Hematology, International University of Health and Welfare, Narita, Chiba, Japan.

Tadashi Matsuda (T)

Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan. Electronic address: tmatsuda@pharm.hokudai.ac.jp.

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Classifications MeSH