The link between menin and pleiotrophin in the tumor biology of pancreatic neuroendocrine neoplasms

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The link between menin and pleiotrophin in the tumor biology of pancreatic neuroendocrine neoplasms. / He, Liping; Boulant, Steeve; Stanifer, Megan; Guo, Cuncai; Nießen, Anna; Chen, Mingyi; Felix, Klaus; Bergmann, Frank; Strobel, Oliver; Schimmack, Simon.

in: CANCER SCI, Jahrgang 113, Nr. 5, 05.2022, S. 1575-1586.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

He, L, Boulant, S, Stanifer, M, Guo, C, Nießen, A, Chen, M, Felix, K, Bergmann, F, Strobel, O & Schimmack, S 2022, 'The link between menin and pleiotrophin in the tumor biology of pancreatic neuroendocrine neoplasms', CANCER SCI, Jg. 113, Nr. 5, S. 1575-1586. https://doi.org/10.1111/cas.15301

APA

He, L., Boulant, S., Stanifer, M., Guo, C., Nießen, A., Chen, M., Felix, K., Bergmann, F., Strobel, O., & Schimmack, S. (2022). The link between menin and pleiotrophin in the tumor biology of pancreatic neuroendocrine neoplasms. CANCER SCI, 113(5), 1575-1586. https://doi.org/10.1111/cas.15301

Vancouver

Bibtex

@article{a7a125d8549242ae9dafdf3adf1571de,
title = "The link between menin and pleiotrophin in the tumor biology of pancreatic neuroendocrine neoplasms",
abstract = "MEN1, which encodes menin protein, is the most frequently mutated gene in pancreatic neuroendocrine neoplasms (pNEN). Pleiotrophin (PTN) has been reported as a downstream factor of menin that promotes metastasis in different tumor entities. In this study, the effect of menin and its link to PTN were assessed using features of pNEN cells and the outcome of patients with pNEN. The expression levels of menin and PTN in tissues from patients with pNEN were examined using qRT-PCR and western blot and compared with their metastasis status. Functional assays, including transwell migration/invasion and scratch wound-healing assays, were performed on specifically designed CRISPR/Cas9-mediated MEN1-knockout (MEN1-KO) pNEN cell lines (BON1MEN1-KO and QGP1MEN1-KO ) to study the metastasis of pNEN. Among 30 patients with menin-negative pNEN, 21 revealed a strong protein expression of PTN. This combination was associated with metastasis and shorter disease-free survival. Accordingly, in BON1MEN1-KO and QGP1MEN1-KO cells, PTN protein expression was positively associated with enhanced cell migration and invasion, which could be reversed using PTN silencing. PTN is a predicting factor of metastatic behavior of menin-deficient-pNEN. In vitro, menin is able to both promote and suppress the metastasis of pNEN by regulating PTN expression depending on the tumoral origin of pNEN cells.",
author = "Liping He and Steeve Boulant and Megan Stanifer and Cuncai Guo and Anna Nie{\ss}en and Mingyi Chen and Klaus Felix and Frank Bergmann and Oliver Strobel and Simon Schimmack",
year = "2022",
month = may,
doi = "10.1111/cas.15301",
language = "English",
volume = "113",
pages = "1575--1586",
journal = "CANCER SCI",
issn = "1347-9032",
publisher = "Wiley-Blackwell",
number = "5",

}

RIS

TY - JOUR

T1 - The link between menin and pleiotrophin in the tumor biology of pancreatic neuroendocrine neoplasms

AU - He, Liping

AU - Boulant, Steeve

AU - Stanifer, Megan

AU - Guo, Cuncai

AU - Nießen, Anna

AU - Chen, Mingyi

AU - Felix, Klaus

AU - Bergmann, Frank

AU - Strobel, Oliver

AU - Schimmack, Simon

PY - 2022/5

Y1 - 2022/5

N2 - MEN1, which encodes menin protein, is the most frequently mutated gene in pancreatic neuroendocrine neoplasms (pNEN). Pleiotrophin (PTN) has been reported as a downstream factor of menin that promotes metastasis in different tumor entities. In this study, the effect of menin and its link to PTN were assessed using features of pNEN cells and the outcome of patients with pNEN. The expression levels of menin and PTN in tissues from patients with pNEN were examined using qRT-PCR and western blot and compared with their metastasis status. Functional assays, including transwell migration/invasion and scratch wound-healing assays, were performed on specifically designed CRISPR/Cas9-mediated MEN1-knockout (MEN1-KO) pNEN cell lines (BON1MEN1-KO and QGP1MEN1-KO ) to study the metastasis of pNEN. Among 30 patients with menin-negative pNEN, 21 revealed a strong protein expression of PTN. This combination was associated with metastasis and shorter disease-free survival. Accordingly, in BON1MEN1-KO and QGP1MEN1-KO cells, PTN protein expression was positively associated with enhanced cell migration and invasion, which could be reversed using PTN silencing. PTN is a predicting factor of metastatic behavior of menin-deficient-pNEN. In vitro, menin is able to both promote and suppress the metastasis of pNEN by regulating PTN expression depending on the tumoral origin of pNEN cells.

AB - MEN1, which encodes menin protein, is the most frequently mutated gene in pancreatic neuroendocrine neoplasms (pNEN). Pleiotrophin (PTN) has been reported as a downstream factor of menin that promotes metastasis in different tumor entities. In this study, the effect of menin and its link to PTN were assessed using features of pNEN cells and the outcome of patients with pNEN. The expression levels of menin and PTN in tissues from patients with pNEN were examined using qRT-PCR and western blot and compared with their metastasis status. Functional assays, including transwell migration/invasion and scratch wound-healing assays, were performed on specifically designed CRISPR/Cas9-mediated MEN1-knockout (MEN1-KO) pNEN cell lines (BON1MEN1-KO and QGP1MEN1-KO ) to study the metastasis of pNEN. Among 30 patients with menin-negative pNEN, 21 revealed a strong protein expression of PTN. This combination was associated with metastasis and shorter disease-free survival. Accordingly, in BON1MEN1-KO and QGP1MEN1-KO cells, PTN protein expression was positively associated with enhanced cell migration and invasion, which could be reversed using PTN silencing. PTN is a predicting factor of metastatic behavior of menin-deficient-pNEN. In vitro, menin is able to both promote and suppress the metastasis of pNEN by regulating PTN expression depending on the tumoral origin of pNEN cells.

U2 - 10.1111/cas.15301

DO - 10.1111/cas.15301

M3 - SCORING: Journal article

C2 - 35179814

VL - 113

SP - 1575

EP - 1586

JO - CANCER SCI

JF - CANCER SCI

SN - 1347-9032

IS - 5

ER -