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Knock-Down of Mucolipin 1 Channel Promotes Tumor Progression and Invasion in Human Glioblastoma Cell Lines.
Santoni, Giorgio; Amantini, Consuelo; Nabissi, Massimo; Maggi, Federica; Arcella, Antonietta; Marinelli, Oliviero; Eleuteri, Anna Maria; Santoni, Matteo; Morelli, Maria Beatrice.
Afiliación
  • Santoni G; Immunopathology Laboratory, School of Pharmacy, University of Camerino, Camerino, Italy.
  • Amantini C; Immunopathology Laboratory, School of Biosciences and Veterinary Medicine, University of Camerino, Camerino, Italy.
  • Nabissi M; Immunopathology Laboratory, School of Pharmacy, University of Camerino, Camerino, Italy.
  • Maggi F; Department of Molecular Medicine, Sapienza University, Rome, Italy.
  • Arcella A; Neuropathology Laboratory, Istituto di Ricovero e Cura a Carattere Scientifico Neuromed, Pozzilli, Italy.
  • Marinelli O; Immunopathology Laboratory, School of Pharmacy, University of Camerino, Camerino, Italy.
  • Eleuteri AM; Clinical Biochemistry Laboratory, School of Biosciences and Veterinary Medicine, University of Camerino, Camerino, Italy.
  • Santoni M; Medical Oncology Unit, Hospital of Macerata, Macerata, Italy.
  • Morelli MB; Immunopathology Laboratory, School of Pharmacy, University of Camerino, Camerino, Italy.
Front Oncol ; 11: 578928, 2021.
Article en En | MEDLINE | ID: mdl-33954107
Among cancers that affect the central nervous system, glioblastoma is the most common. Given the negative prognostic significance of transient receptor potential mucolipin 1 (TRPML1) channel reduction in patients with glioblastoma, as discussed in previous publications, the aim of the current study was to investigate the biological advantage of TRPML1 loss for glioma cells. Human glioblastoma primary cancer cells (FSL and FCL) and glioblastoma cell lines (T98 and U251) were used for that purpose. TRPML1 silencing in T98 cells induces defective autophagy, nitric oxide (NO) production, and cathepsin B-dependent apoptosis in the first 48 h and then apoptotic-resistant cells proliferate with a high growth rate with respect to control cells. In U251 cells, knock-down of TRPML1 stimulates NO generation and protein oxidation, arrests cell cycle at G2/M phase, and induces autophagy leading to cathepsin B-dependent senescence. Finally, in both cell lines, the long-term effects of TRPML1 silencing promote survival and invasion capacity with respect to control cells. Silencing of TRPML1 also affects the phenotype of glioblastoma primary cells. FSL cells show increased proliferation ability, while FCL cells enter into senescence associated with an increased invasion ability. In conclusion, although the molecular heterogeneity among different glioblastoma cell lines mirrors the intercellular heterogeneity in cancer cells, our data support TRPML1 downregulation as a negative prognostic factor in glioblastoma.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: Front Oncol Año: 2021 Tipo del documento: Article País de afiliación: Italia Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: Front Oncol Año: 2021 Tipo del documento: Article País de afiliación: Italia Pais de publicación: Suiza