Dysregulated splicing factor SF3B1 unveils a dual therapeutic vulnerability to target pancreatic cancer cells and cancer stem cells with an anti-splicing drug.

Emilia Alors-PerezRicardo Blázquez-EncinasSonia AlcaláCristina Viyuela-GarcíaSergio Pedraza-ArevaloVicente Herrero-AguayoJuan M Jiménez-VacasAndrea MafficiniMarina E Sánchez-FríasMaría T CanoFernando Abollo-JiménezJuan A Marín-SanzPablo Cabezas-SainzRita T LawlorClaudio LuchiniLaura SánchezJuan M Sánchez-HidalgoSebastián VenturaLaura Martin-HijanoManuel D GaheteAldo ScarpaÁlvaro Arjona-SánchezAlejandro Ibáñez-CostaBruno SainzRaúl M LuqueJusto P. Castaño

Published in: Journal of experimental & clinical cancer research : CR (2021)

SF3B1 overexpression represents a therapeutic vulnerability in PDAC, as altered splicing can be targeted with Pladienolide-B both in cancer cells and CSCs, paving the way for novel therapies for this lethal cancer.

Keyphrases

cancer stem cells
climate change
papillary thyroid
cell proliferation
squamous cell
transcription factor
adverse drug