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  • 1. Berg Nordstrand, Laila
    et al.
    Pinheiro, Rómulo
    Geschwind, Lars
    KTH, Skolan för teknikvetenskaplig kommunikation och lärande (ECE), Lärande.
    Vrangbæk, Karsten
    Responses to the Global Financial Crisis: Lessons From the Public Sector in the Nordic Countries2017Inngår i: Scandinavian Journal of Public Administration, ISSN 2001-7405, E-ISSN 2001-7413, Vol. 21, nr 1, s. 3-8Artikkel i tidsskrift (Fagfellevurdert)
  • 2.
    Poutanen, Mikko
    et al.
    Faculty of Management and Business, Tampere University, Finland.
    Tervasmaki, Tuomas
    Faculty of Education and Culture, Tampere University, Finland.
    Pinheiro, Rómulo
    Department of Political Science and Management, University of Agder, Norway.
    Geschwind, Lars
    KTH, Skolan för industriell teknik och management (ITM), Lärande, Lärande i Stem.
    SJPA Special Issue Introduction: What Has Changed and What Remains? Institutional Shifts in Nordic Higher Education in the 2000s2023Inngår i: Scandinavian Journal of Public Administration, ISSN 2001-7405, E-ISSN 2001-7413, Vol. 27, nr 1, s. 1-7Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    NDFIP1 has been previously reported as a tumor suppressor in multiple solid tumors, but the function of NDFIP1 in NSCLC and the underlying mechanism are still unknown. Besides, the WW domain containing proteins can be recognized by NDFIP1, resulted in the loading of the target proteins into exosomes. However, whether WW domain-containing transcription regulator 1 (WWTR1, also known as TAZ) can be packaged into exosomes by NDFIP1 and if so, whether the release of this oncogenic protein via exosomes has an effect on tumor development has not been investigated to any extent. Here, we first found that NDFIP1 was low expressed in NSCLC samples and cell lines, which is associated with shorter OS. Then, we confirmed the interaction between TAZ and NDFIP1, and the existence of TAZ in exosomes, which requires NDFIP1. Critically, knockout of NDFIP1 led to TAZ accumulation with no change in its mRNA level and degradation rate. And the cellular TAZ level could be altered by exosome secretion. Furthermore, NDFIP1 inhibited proliferation in vitro and in vivo, and silencing TAZ eliminated the increase of proliferation caused by NDFIP1 knockout. Moreover, TAZ was negatively correlated with NDFIP1 in subcutaneous xenograft model and clinical samples, and the serum exosomal TAZ level was lower in NSCLC patients. In summary, our data uncover a new tumor suppressor, NDFIP1 in NSCLC, and a new exosome-related regulatory mechanism of TAZ.

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