ArticleCancer immunology, immunotherapy : CII2022
Endoplasmic reticulum stress-induced release and binding of calreticulin from human ovarian cancer cells.
Article in Cancer immunology, immunotherapy : CII, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- The interaction between endoplasmic reticulum stress and ferroptosis in ovarian diseases.Journal of ovarian research · 2026Pooled it
- A chemical-genetic system for calreticulin exposure on cancer cells reveals immune-dependent antitumor effects.Cell death and differentiation · 2026Article
- Nanoparticles co-loaded with bacillus Calmette-Guérin pure protein derivative and doxorubicin for bladder tumor therapy.BMC biotechnology · 2026Article
- IL-24 amplifies baicalein-induced immunogenic cell death in ovarian cancer by boosting endoplasmic reticulum stress.Journal of ovarian research · 2026Article
- Smad7 is a negative regulator of immunogenic cell death in colorectal cancer.Oncoimmunology · 2025Article
- Tauroursodeoxycholic acid-induced increase in ectopic muscle mineralization occurs exclusively in dystrophic muscles and is independent of endoplasmic reticulum stress.Scientific reports · 2025Article
- Apoptosis-inducing activity of a steroidal glycoside from Allium chinense G. Don. bulbs in human small-cell lung cancer cells via mitochondrial dysfunction and ER stress.Journal of natural medicines · 2025Article
- Nanoparticle-mediated celastrol ER targeting delivery amplify immunogenic cell death in melanoma.Journal of advanced research · 2025Article
- Discovery of a Chimeric Polyketide Family as Cancer Immunogenic Chemotherapeutic Leads.Journal of the American Chemical Society · 2025Article
- Endoplasmic reticulum stress in non-small cell lung cancer.American journal of cancer research · 2025Review
- O-GlcNAcylation in ovarian tumorigenesis and its therapeutic implications.Translational oncology · 2025Review
- Response to Neoadjuvant Chemotherapy in Invasive Breast Cancer Predicted by CD4+, CD8+, and FOXP3+ Tumor-Infiltrating Lymphocytes.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- Endoplasmic reticulum stress response pathway-mediated cell death in ovarian cancer.Frontiers in oncology · 2024Review
- Targeting endoplasmic reticulum associated degradation pathway combined with radiotherapy enhances the immunogenicity of esophageal cancer cells.Cancer biology & therapy · 2023Article
- Intricate subcellular journey of nanoparticles to the enigmatic domains of endoplasmic reticulum.Drug delivery · 2023Review
- Targeting endoplasmic reticulum stress signaling in ovarian cancer therapy.Cancer biology & medicine · 2023Review
- Calreticulin as a marker and therapeutic target for cancer.Clinical and experimental medicine · 2023Review
- In Situ Vaccination with Mitochondria-Targeting Immunogenic Death Inducer Elicits CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The therapeutic mavericks: Potent immunomodulating chaperones capable of treating human diseases.Journal of cellular and molecular medicine · 2023Review
- 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
6 authors at 4 institutions in 5 countries.
Funding
Abstract
backgroundCalreticulin (CRT) is an endoplasmic reticulum (ER) chaperone, but can appear surface bound on cancers cells, including ovarian cancers (OC). We investigated at what stage of cell viability, CRT appeared associated with surface of human OC cells. CRT on pre-apoptotic tumour cells is thought to initiate their eradication via a process termed immunogenic cell death (ICD).
methodsWe treated OC cells with the chemotherapeutic-doxorubicin (DX) known to induce translocation of CRT to some tumour cell surfaces, with and without the ER stressor-thapsigargin (TG)-and/or an ER stress inhibitor-TUDCA. We monitored translocation/release of CRT in pre-apoptotic cells by flow cytometry, immunoblotting and ELISA. We investigated the difference in binding of FITC-CRT to pre-apoptotic, apoptotic and necrotic cells and the ability of extracellular CRT to generate immature dendritic cells from THP-1 monocytes.
resultsDx-treatment increased endogenously released CRT and extracellular FITC_CRT binding to human pre-apoptotic OC cells. DX and TG also promoted cell death in OC cells which also increased CRT release. These cellular responses were significantly inhibited by TUDCA, suggesting that ER stress is partially responsible for the changes in CRT cellular distribution. Extracellular CRT induces maturation of THP-1 towards a imDC phenotype, an important component of ICD.
conclusionCollectively, these cellular responses suggest that ER stress is partially responsible for the changes in CRT cellular distribution. ER-stress regulates in part the release and binding of CRT to human OC cells where it may play a role in ICD.
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Registered trials
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