Deregulation of linc-PINT in acute lymphoblastic leukemia is implicated in abnormal proliferation of leukemic cells

Long Non-Coding RNAs (lncRNAs) are functional RNAs longer than 200 nucleotides in length. Several lncRNAs are involved in cell proliferation and are deregulated in several human tumors. Few lncRNAs have been described to play a role in Acute Lymphoblastic Leukemia (ALL). In this study, we carried ou...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Oncotarget 2018-02, Vol.9 (16), p.12842-12852
Hauptverfasser: Garitano-Trojaola, Andoni, José-Enériz, Edurne San, Ezponda, Teresa, Unfried, Juan Pablo, Carrasco-León, Arantxa, Razquin, Nerea, Barriocanal, Marina, Vilas-Zornoza, Amaia, Sangro, Bruno, Segura, Victor, Prósper, Felipe, Fortes, Puri, Agirre, Xabier
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Long Non-Coding RNAs (lncRNAs) are functional RNAs longer than 200 nucleotides in length. Several lncRNAs are involved in cell proliferation and are deregulated in several human tumors. Few lncRNAs have been described to play a role in Acute Lymphoblastic Leukemia (ALL). In this study, we carried out a genome wide lncRNA expression profiling in ALL samples and peripheral blood samples obtained from healthy donors. We detected 43 lncRNAs that were aberrantly expressed in ALL. Interestingly, among them, showed a significant downregulation in T and B-ALL. Re-expression of in ALL cells induced inhibition of leukemic cell growth that was associated with apoptosis induction and cell cycle arrest in G /M phase. induced the transcription of which reduced the viability of ALL cells. Intriguingly, we observed that treatment with anti-tumoral epigenetic drugs like LBH-589 (Panobinostat) and Curcumin induced the expression of and in ALL. These results indicate that the downregulation of plays a relevant role in the pathogenesis of ALL, and re-expression may be one of the mechanisms exerted by epigenetic drugs to reduce cell proliferation in ALL.
ISSN:1949-2553
1949-2553
DOI:10.18632/oncotarget.24401