Overexpression of TC-PTP in murine epidermis attenuates skin tumor formation.


Journal

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

Informations de publication

Date de publication:
05 2020
Historique:
received: 26 03 2019
accepted: 23 03 2020
revised: 18 03 2020
pubmed: 15 4 2020
medline: 25 11 2020
entrez: 15 4 2020
Statut: ppublish

Résumé

T-cell protein tyrosine phosphatase (TC-PTP), encoded by Ptpn2, has been shown to function as a tumor suppressor during skin carcinogenesis. In the current study, we generated a novel epidermal-specific TC-PTP-overexpressing (K5HA.Ptpn2) mouse model to show that TC-PTP contributes to the attenuation of chemically induced skin carcinogenesis through the synergistic regulation of STAT1, STAT3, STAT5, and PI3K/AKT signaling. We found overexpression of TC-PTP increased epidermal sensitivity to DMBA-induced apoptosis and it decreased TPA-mediated hyperproliferation, coinciding with reduced epidermal thickness. Inhibition of STAT1, STAT3, STAT5, or AKT reversed the effects of TC-PTP overexpression on epidermal survival and proliferation. Mice overexpressing TC-PTP in the epidermis developed significantly reduced numbers of tumors during skin carcinogenesis and presented a prolonged latency of tumor initiation. Examination of human papillomas and squamous cell carcinomas (SCCs) revealed that TC-PTP expression was significantly reduced and TC-PTP expression was inversely correlated with the increased grade of SCCs. Our findings demonstrate that TC-PTP is a potential therapeutic target for the prevention of human skin cancer given that it is a major negative regulator of oncogenic signaling.

Identifiants

pubmed: 32286519
doi: 10.1038/s41388-020-1282-8
pii: 10.1038/s41388-020-1282-8
pmc: PMC7244373
mid: NIHMS1579167
doi:

Substances chimiques

Neoplasm Proteins 0
PTPN2 protein, human EC 3.1.3.48
Protein Tyrosine Phosphatase, Non-Receptor Type 2 EC 3.1.3.48
Ptpn2 protein, mouse EC 3.1.3.48

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

4241-4256

Subventions

Organisme : NIEHS NIH HHS
ID : R01 ES022250
Pays : United States

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Auteurs

Mihwa Kim (M)

Department of Molecular Science, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, USA.

Liza D Morales (LD)

Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, USA.

Cheol Jung Lee (CJ)

Department of Molecular Science, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, USA.

Serena A Olivarez (SA)

Department of Molecular Science, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, USA.

Woo Jin Kim (WJ)

School of Mathematical and Statistical Sciences, College of Sciences, University of Texas Rio Grande Valley, Edinburg, TX, USA.

Joselin Hernandez (J)

Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, USA.

Srinivas Mummidi (S)

Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, USA.

Christopher Jenkinson (C)

Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, USA.

Andrew T Tsin (AT)

Department of Molecular Science, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, USA.

Ik-Soon Jang (IS)

Division of Bioconvergence Analysis, Korea Basic Science Institute, Daejeon, 305-333, Republic of Korea.

Thomas J Slaga (TJ)

Department of Pharmacology, School of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.

Dae Joon Kim (DJ)

Department of Molecular Science, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, USA. dae.kim@utrgv.edu.
Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Edinburg, TX, USA. dae.kim@utrgv.edu.

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