ArticleOncotarget2017
Endoplasmic reticulum stress-mediated membrane expression of CRT/ERp57 induces immunogenic apoptosis in drug-resistant endometrial cancer cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Doxorubicin induces ferroptosis in endometrial cancer by suppressing the MKK6/p38/CEBPB axis.Journal of translational medicine · 2026Article
- Key Tumor Responsive ZIF-8 Nanocarriers for Effective Anti-Cancer Therapeutics.International journal of nanomedicine · 2026Review
- Immunogenic Cell Death Traits Emitted from Chronic Lymphocytic Leukemia Cells Following Treatment with a Novel Anti-Cancer Agent, SpiD3.Biomedicines · 2024Article
- Stressed target cancer cells drive nongenetic reprogramming of CAR T cells and solid tumor microenvironment.Nature communications · 2023Article
- Stressed target cancer cells drive nongenetic reprogramming of CAR T cells and tumor microenvironment, overcoming multiple obstacles of CAR T therapy for solid tumors.Research square · 2023Article
- Trial watch: chemotherapy-induced immunogenic cell death in oncology.Oncoimmunology · 2023Review
- Chemotherapeutic and targeted drugs-induced immunogenic cell death in cancer models and antitumor therapy: An update review.Frontiers in pharmacology · 2023Review
- Article
- Expression of apoptosis-related proteins in the pathogenesis of endometrial clear cell carcinoma.International journal of clinical and experimental pathology · 2022Article
- Dexmedetomidine Preconditioning Reduces Myocardial Ischemia-Reperfusion Injury in Rats by Inhibiting the PERK Pathway.Arquivos brasileiros de cardiologia · 2021Article
- Unraveling the regulatory role of endoplasmic-reticulum-associated degradation in tumor immunity.Critical reviews in biochemistry and molecular biology · 2020Review
- Review
- RIG-I promotes IFN/JAK2 expression and the endoplasmic reticulum stress response to inhibit chemoradiation resistance in nasopharyngeal carcinoma.Cancer medicine · 2019Article
- Endoplasmic reticulum stress enhances the antigen-specific T cell immune responses and therapeutic antitumor effects generated by therapeutic HPV vaccines.Journal of biomedical science · 2019Article
- Unfolded protein response complexity in gynecological tumor dynamics: therapeutic challenges and future perspectives.Cell cycle (Georgetown, Tex.)Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the role of endoplasmic reticulum (ER) stress-mediated CRT/ERp57 complex expression underlying the mechanism of resistance to doxorubicin (DOX) in endometrial carcinoma (EC)
methodsThe expression of CRT, ERp57, p-PERK, eIF2α, p-eIF2α in EC patients and EC cells was detected by Western blots and by immunofluorescence assay. MTT assay was used to determine the LC50 of EC cells to DOX and cell viability. Apoptosis was assayed using flow cytometer. The protein expression of PERK, cleaved-caspase-8, p-eIF2α and CHOP were detected by Western blot, and the expression of VAMP-1, SNAP23 and PERK was knockdown by siRNA and/or shRNA. The expression of CRT/ERp57 complex was detected by flow cytometry. In addition, the expression of eIF2α and p-eIF2α was detected by Western blot analysis after drug-resistant EC cells were transfected with lentivirus overexpressing CRT, treated with GADD34 inhibitor and ES stress inducer. MTT assay was used to detect the phagocytic activity of T cells induced by maturation of dendritic cells in drug-resistant EC cells.
resultsThe expression of CRT, ERp57, p-PERK and p-eIF2α was significantly decreased in the drug-resistant patients in EC patients. The IC
conclusionDOX can induce the death of tumor cells by ER stress-mediated CRT/ERp57 expression in EC cells. Induction of ER stress in drug-resistant EC cells up-regulates the membrane expression of CRT/ERp57, enhances phagocytosis, induces immunogenic apoptosisand sensitizes the cells to DOX.
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