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Título

The immunoglobulin-like domain of neuregulins potentiates ErbB3/HER3 activation and cellular proliferation

AutorCenta, Ariana; Rodríguez-Barrueco, Ruth CSIC ORCID; Montero, Juan Carlos CSIC ORCID; Pandiella, Atanasio CSIC ORCID CVN
Palabras claveBreast cancer
HER receptors
Ig-like domain
Neuregulins
Fecha de publicaciónjun-2018
EditorJohn Wiley & Sons
CitaciónMolecular Oncology 12(7): 1061-1076 (2018)
ResumenThe neuregulins (NRGs) represent a large family of membrane-anchored growth factors, whose deregulation may contribute to the pathogenesis of several tumors. In fact, targeting of NRG-activated pathways has demonstrated clinical benefit. To improve the efficacy of anti-NRG therapies, it is essential to gain insights into the regions of NRGs that favor their pro-oncogenic properties. Here, we have addressed the protumorigenic impact of different NRG domains. To do this, deletion mutants affecting different NRG domains were expressed in 293 and MCF7 cells. Of the five forms studied, only the wild-type and a mutant lacking the Ig-like domain (NRGΔIg) were properly sorted to the plasma membrane. Both forms were released as soluble forms to the culture media. However, the mutant NRGΔIg failed to efficiently activate HER2 and HER3 receptors, signaling pathways, and cell proliferation when compared to wild-type NRG. Treatment with trastuzumab, a humanized antibody used in the breast cancer clinic, inhibited the constitutive activation of HER2, HER3, and downstream signaling in MCF7 cells constitutively expressing wild-type NRG. In contrast, this treatment had a marginal effect on MCF7-NRGΔIg cells. This study demonstrates that the Ig-like region of NRGs exerts an important role in their capability to activate ErbB/HER receptors and mitogenic responses. Strategies aimed at targeting NRGs should consider that fact to improve neutralization of the pro-oncogenic properties of NRGs.
Descripción© 2018 The Authors.
Versión del editorhttp://dx.doi.org/10.1002/1878-0261.12310
URIhttp://hdl.handle.net/10261/245398
DOI10.1002/1878-0261.12310
ISSN1878-0261
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