Targeting COPZ1 non-oncogene addiction counteracts the viability of thyroid tumor cells

Alessandro Gulino, Claudio Tripodo, Beatrice Belmonte, Katia Todoerti, Daniele Lecis, Maria Chiara Anania, Giacomo Manenti, Elena Cetti, Giuseppe Mauro, Tiziana Di Marco, Antonino Neri, Giacomo Manenti, Loredana Cleris, Sonia Pagliardini, Giacomo Manenti, Angela Greco

Risultato della ricerca: Articlepeer review

11 Citazioni (Scopus)


Thyroid carcinoma is generally associated with good prognosis, but no effective treatments are currently available for aggressive forms not cured by standard therapy. To find novel therapeutic targets for this tumor type, we had previously performed a siRNA-based functional screening to identify genes essential for sustaining the oncogenic phenotype of thyroid tumor cells, but not required to the same extent for the viability of normal cells (non-oncogene addiction paradigm). Among those, we found the coatomer protein complex ζ1 (COPZ1) gene, which is involved in intracellular traffic, autophagy and lipid homeostasis. In this paper, we investigated the mechanisms through which COPZ1 depletion leads to thyroid tumor cell death. We showed that siRNA-mediated COPZ1 depletion causes abortive autophagy, endoplasmic reticulum stress, unfolded protein response and apoptosis. Interestingly, we observed that mouse tumor xenografts, locally treated with siRNA targeting COPZ1, showed a significant reduction of tumor growth. On the whole, we demonstrated for the first time the crucial role of COPZ1 in the viability of thyroid tumor cells, suggesting that it may be considered an attractive target for novel therapeutic approaches for thyroid cancer.
Lingua originaleEnglish
pagine (da-a)201-211
Numero di pagine11
RivistaCancer Letters
Stato di pubblicazionePublished - 2017

All Science Journal Classification (ASJC) codes

  • ???subjectarea.asjc.2700.2730???
  • ???subjectarea.asjc.1300.1306???


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