{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["22(1)"],"submitter":["Chen CY"],"pubmed_abstract":["Endoplasmic reticulum (ER) stress response is an adaptive program to cope with cellular stress that disturbs the function and homeostasis of ER, which commonly occurs during cancer progression to late stage. Late-stage cancers, mostly requiring chemotherapy, often develop treatment resistance. Chemoresistance has been linked to ER stress response; however, most of the evidence has come from studies that correlate the expression of stress markers with poor prognosis or demonstrate proapoptosis by the knockdown of stress-responsive genes. Since ER stress in cancers usually persists and is essentially not induced by genetic manipulations, we used low doses of ER stress inducers at levels that allowed cell adaptation to occur in order to investigate the effect of stress response on chemoresist"],"journal":["International journal of molecular sciences"],"pagination":["E355"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7794796"],"repository":["biostudies-literature"],"pubmed_title":["Adaptation to Endoplasmic Reticulum Stress Enhances Resistance of Oral Cancer Cells to Cisplatin by Up-Regulating Polymerase η and Increasing DNA Repair Efficiency."],"pmcid":["PMC7794796"],"pubmed_authors":["Poon CL","Lin YS","Wu PJ","Chen BH","Chen YC","Weng RR","Kawasumi M","Hung KF","Chen CY","Lan TY","Wu CH","Lo JF","Sun YC"],"additional_accession":[]},"is_claimable":false,"name":"Adaptation to Endoplasmic Reticulum Stress Enhances Resistance of Oral Cancer Cells to Cisplatin by Up-Regulating Polymerase η and Increasing DNA Repair Efficiency.","description":"Endoplasmic reticulum (ER) stress response is an adaptive program to cope with cellular stress that disturbs the function and homeostasis of ER, which commonly occurs during cancer progression to late stage. Late-stage cancers, mostly requiring chemotherapy, often develop treatment resistance. Chemoresistance has been linked to ER stress response; however, most of the evidence has come from studies that correlate the expression of stress markers with poor prognosis or demonstrate proapoptosis by the knockdown of stress-responsive genes. Since ER stress in cancers usually persists and is essentially not induced by genetic manipulations, we used low doses of ER stress inducers at levels that allowed cell adaptation to occur in order to investigate the effect of stress response on chemoresist","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Dec","modification":"2025-04-26T02:05:48.93Z","creation":"2021-02-20T20:51:33Z"},"accession":"S-EPMC7794796","cross_references":{"pubmed":["33396303"],"doi":["10.3390/ijms22010355"]}}