6533b7ddfe1ef96bd127474b

RESEARCH PRODUCT

Obese rats exhibit high levels of isoprostanes in acute pancreatitis

J EscobarJavier PeredaD. RoyoJuan SastreLuis SabaterSalvador PérezLuis AparisiMiguel Asensi

subject

Messenger RNAHepatologybusiness.industryEndocrinology Diabetes and MetabolismCellAlternative splicingGastroenterologyCancermedicine.diseaseGemcitabinemedicine.anatomical_structurePancreatic cancerRNA splicingmedicineCancer researchEpithelial–mesenchymal transitionbusinessmedicine.drug

description

s / Pancreatology 12 (2012) 502–597 538 interference of Sam68 and SRSF1 expression cause a partial recovery of drug sensitivity. Conclusions: Our results show that chronic exposure of PDAC cells to gemcitabine leads to selection of a drug-resistant subpopulation overexpressing Sam68 and SRSF1. Importantly, the depletion of these proteins leads to a partial recovery of the sensibility to gemcitabine, suggesting that they may represent suitable molecular-targets to overcome drug resistance in PDAC. Arumugam T, Ramachandran V, Fournier KF, et al. Epithelial to mesenchymal transition contributes to drug resistance in pancreatic cancer. Cancer Res. 2009 Jul Shapiro IM, Cheng AW, Flytzanis NC, et al. An EMT-driven alternative splicing program occurs in human breast cancer and modulates cellular phenotype. PLoS Genet. 2011 Ghigna C, De Toledo M, Bonomi S, et al. Pro-metastatic splicing of Ron proto-oncogene mRNA can be reversed: therapeutic potential of bifunctional oligonucleotides and indole derivatives. RNA Biol. 2010 Valacca C, Bonomi S, Buratti E, et al. Sam68 regulates EMT through alternative splicing-activated nonsense-mediated mRNA decay of the SF2/ASF proto-oncogene. J Cell Biol. 2010

yearjournalcountryeditionlanguage
2012-11-01Pancreatology
https://doi.org/10.1016/j.pan.2012.11.127