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ABTL0812 enhances antitumor effect of paclitaxel and reverts chemoresistance in triple-negative breast cancer models

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Cancer Communications 2022年第6期42卷 567-571页

作者： Emma Polonio-Alcala Sònia Solé-Sánchez pau munoz-guardiola Elisabet Megías-Roda Héctor Perez-Montoyo Marc Yeste-Velasco Jose Alfón Jose Miguel Lizcano Carles Domènech Santiago Ruiz-Martínez Teresa Puig New Therapeutic Targets Laboratory(TargetsLab)-Oncology Unit Department of Medical SciencesUniversity of GironaGirona 17003Spain Product Process and Production Engineering Research Group(GREP)Department of Mechanical Engineering and Industrial ConstructionUniversity of GironaGirona 17003Spain Ability Pharmaceuticals SLCerdanyola del VallesBarcelona 08290Spain Protein Kinases and Signal Transduction Laboratory Department de Bioquimica i Biologia Molecular and Institut de NeurocienciesUniversitat Autonoma de BarcelonaBellaterraBarcelona 08193Spain

Dear Editor,Triple-negative breast cancer(TNBC)accounts for 20%of all breast carcinomas and lacks a validated targeted therapy;thus,currently,cytotoxic chemotherapy is the treatment of choice[1].Compared with other breast cancer types,patientswith TNBCare younger,have larger tumors,a higher risk of metastasis,and a higher rate of recurrence[2].Among all the subtypes described by Lehmann et al.[3],mesenchymal-like and mesenchymal stem-like(MSL)subtypes had the lowest 5-year distant metastasis-free survival rates.

关键词： ABTL0812 TRIB3 Autophagy Breast Cancer Targeted Therapy Chemoresistance

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PKR and PP1C Polymorphisms in Alzheimer’s Disease Risk

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Neuroscience & Medicine 2011年第3期2卷 226-231页

作者： Ernest Palomer Gerard ILL-Raga Marta Tajes Eva Ramos-Fernández Mònica Bosch-Morató Biuse Guivernau Jose J.Galan Jordi Clarimon Carmen Antunez Merce Boada Luis M.Real César Fandos Francisco J.munoz Laboratory of Molecular Physiology and Channelopathies Department of Experimental and Health SciencesPompeu Fabra University(UPF)BarcelonaSpain NeoCodex SevillaSpain Alzheimer Laboratory Neurology DepartmentSanta Creu and Sant Pau HospitalBiomedical Research Center on Neurodegenerative Diseases(CIBERNED)BarcelonaSpain Fundacion Alzheimur Dementia UnitVirgen de la Arrixaca HospitalMurciaSpain Memory Clinic of ACE Foundation Catalan Institute of Applied NeurosciencesBarcelonaSpain Neurology Department Vall d’Hebron Universitary HospitalBarcelonaSpain

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by senile plaques and neurofibrillary tangles. Senile plaques are deposits of amyloid ?-peptide (A?) produced by the cleavage of a transmembrane protein termed Amyloid Precursor Protein (APP). The amyloidogenic cleavage of APP is performed by γ-secretase complex and ?-site APP cleaving enzyme 1 (BACE1), a key enzyme in AD that can be activated by different noxious stimuli. Interestingly, some viruses could activate double-stranded RNA-activated protein kinase (PKR), which phosphorylates Eukaryotic Initiation Factor 2 alpha (eIF2α). This phosphorylation stops global translation to avoid any synthesis of viral infective proteins, but paradoxically up-regulates BACE1 translation. One of the viral mechanisms to circumvent eIF2α phosphorylation is the recruitment of protein phosphatase 1 (PP1), to fully dephosphorylate eIF2α and allow viral protein synthesis. Due to the functional relationship between BACE1, PKR, PP1 and AD we have performed a large (1122 cases and 1191 control individuals) case-control genetic analysis using two biallelic polymorphisms rs2254958 and rs7480390, located within the genes coding for PKR and the catalytic unit A of PP1, respectively. Although a trend to association of the rs2254958 TT genotype with AD risk was found, our results show that neither rs7480390 nor rs2254958 are associated with AD susceptibility.

关键词： Alzheimer’s Disease BACE1 PKR PP1 eIF2α

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