ArticlePLoS biology2019
Calreticulin is a Critical Cell Survival Factor in Malignant Neoplasms.
Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
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- The examination of in vitro photosensitizing efficacy of aloe-emodin loaded liposome following photodynamic therapy on melanoma cell lines.Scientific reports · 2025Article
- Targeting CALR reduces energy metabolism of esophageal cancer cells and inhibits tumor‑associated fibroblast infiltration.International journal of oncology · 2025Article
- DNA polymerase beta connects tumorigenicity with the circadian clock in liver cancer through the epigenetic demethylation of Per1.Cell death & disease · 2024Article
- The Prognostic Value and Potential Immune Mechanisms of lncRNAs Related to Immunogenic Cell Death in Papillary Thyroid Carcinoma.Journal of inflammation research · 2024Article
- Calreticulin as a marker and therapeutic target for cancer.Clinical and experimental medicine · 2023Review
- ARL-17477 is a dual inhibitor of NOS1 and the autophagic-lysosomal system that prevents tumor growth in vitro and in vivo.Scientific reports · 2023Article
- M2 macrophages drive leukemic transformation by imposing resistance to phagocytosis and improving mitochondrial metabolism.Science advances · 2023Article
- The Double-Edged Proteins in Cancer Proteomes and the Generation of Induced Tumor-Suppressing Cells (iTSCs).Proteomes · 2023Review
- Low-intensity focused ultrasound targeted microbubble destruction reduces tumor blood supply and sensitizes anti-PD-L1 immunotherapy.Frontiers in bioengineering and biotechnology · 2023Article
- Design and characterization of PROTAC degraders specific to protein N-terminal methyltransferase 1.European journal of medicinal chemistry · 2022Article
- Radiosensitization of calreticulin-overexpressing human glioma cell line by the polyphenolic acetate 7, 8-diacetoxy-4-methylcoumarin.Cancer reports (Hoboken, N.J.) · 2022Article
- Endoplasmic reticulum stress-induced release and binding of calreticulin from human ovarian cancer cells.Cancer immunology, immunotherapy : CII · 2022Article
- Ecto-calreticulin expression in multiple myeloma correlates with a failed anti-tumoral immune response and bad prognosis.Oncoimmunology · 2022Article
- Advances in Intracellular Calcium Signaling Reveal Untapped Targets for Cancer Therapy.Biomedicines · 2021Review
- Role and mechanism of chaperones calreticulin and ERP57 in restoring trafficking to mutant HERG‑A561V protein.International journal of molecular medicine · 2021Article
- Gliosarcoma vs. glioblastoma: a retrospective case series using molecular profiling.BMC neurology · 2021Article
- Restoring the Immunity in the Tumor Microenvironment: Insights into Immunogenic Cell Death in Onco-Therapies.Cancers · 2021Review
- Anti-leukemia effect associated with down-regulated CD47 and up-regulated calreticulin by stimulated macrophages in co-culture.Cancer immunology, immunotherapy : CII · 2021Article
- Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Calreticulin (CRT) is a high-capacity Ca2+ protein whose expression is up-regulated during cellular transformation and is associated with disease progression in multiple types of malignancies. At the same time, CRT has been characterized as an important stress-response protein capable of inducing immunogenic cell death (ICD) when translocated to the cell surface. It remains unclear why CRT expression is preserved by malignant cells during the course of transformation despite its immunogenic properties. In this study, we identify a novel, critical function of CRT as a cell survival factor in multiple types of human solid-tissue malignancies. CRT knockdown activates p53, which mediates cell-death response independent of executioner caspase activity and accompanied full-length poly ADP ribose polymerase (PARP) cleavage. Mechanistically, we show that down-regulation of CRT results in mitochondrial Ca2+ overload and induction of mitochondria permeability transition pore (mPTP)-dependent cell death, which can be significantly rescued by the mPTP inhibitor, Cyclosporin A (CsA). The clinical importance of CRT expression was revealed in the analysis of the large cohort of cancer patients (N = 2,058) to demonstrate that high levels of CRT inversely correlates with patient survival. Our study identifies intracellular CRT as an important therapeutic target for tumors whose survival relies on its expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.