Induced mitochondrial deficit by NDUFS3 transient silencing reduces RAB7 expression and causes lysosomal dysfunction in pancreatic cancer cells
Overall, our data show that mitochondrial deficit determines alterations of the crosstalk with lysosomes, leading to dysfunctions, and that this process is regulated by RAB7 acting as an oncogene. This highlights the synergic role of RAB7 and mitochondrial dysfunction, focusing on a cellular mechanism that may boost the effect of mitochondrial dysfunction in the cells, leading to the reduction of the tumorigenic potential.
Authors
- Cecilia Bucci (ORCID: https://orcid.org/0000-0002-6232-6183)
- Paola Cordella
- Roberta Romanò (ORCID: https://orcid.org/0000-0002-4987-3561)
- Sinforosa Gagliardi (ORCID: https://orcid.org/0000-0001-5119-1175)
- Riccardo Di Corato (ORCID: https://orcid.org/0000-0002-7173-6176)
- Giulia Girolimetti (ORCID: https://orcid.org/0000-0001-8917-3634)
- Flora Guerra (ORCID: https://orcid.org/0000-0003-3379-7469)
- Grazia Bramato
Institutions
- University of Salento (IT)
- Center for Biomolecular Nanotechnologies (IT)
- Institute for Microelectronics and Microsystems (IT)
Publication Details
- Journal
- Cell Communication and Signaling
- Published
- 2025-05-14
- DOI
- https://doi.org/10.1186/s12964-025-02214-y
- Citations
- 1
- Primary Topic
- Autophagy in Disease and Therapy
- Type
- article
- Field-Weighted Citation Impact
- 1.35
Funders
- Associazione Italiana per la Ricerca sul Cancro