ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2014
Remodelling of Ca2+ transport in cancer: how it contributes to cancer hallmarks?
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
114 citing papers in PubMed, 1 synthesis or guideline pooled it, 235 citations in OpenAlex.
- The Impact of TRPV1 on Cancer Pathogenesis and Therapy: A Systematic Review.International journal of biological sciences · 2021Pooled it
- UPR/ATF4/Noxa pathway overactivation through SERCA2 inhibition or ONC201 treatment combined with ABT-737 triggers apoptosis in chemoresistant ovarian cancer cells and patient-derived tumor organoids.Cell death & disease · 2026Article
- Fabrication of docetaxel-loaded PEG-modified calcium carbonate-loaded zeolite imidazole nanoframeworks for synergic gastric cancer photothermal therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Transcriptional and epigenetic regulation of CaBioinformatics advances · 2026Article
- OZ-001 Suppresses the Growth of Triple-Negative Breast Cancer and Pancreatic Cancer by Targeting STAT3 Phosphorylation and the Calcium Signaling Pathway.Biomolecules & therapeutics · 2025Article
- Article
- The first-line antihypertensive nitrendipine potentiated the therapeutic effect of oxaliplatin by downregulating CACNA1D in colorectal cancer.Open medicine (Warsaw, Poland) · 2025Article
- Association between dysregulated expression of CaFrontiers in bioinformatics · 2025Article
- The IPBiochimica et biophysica acta. Molecular basis of disease · 2025Article
- The mechanopathology of the tumor microenvironment: detection techniques, molecular mechanisms and therapeutic opportunities.Frontiers in cell and developmental biology · 2025Review
- Prognostic value ofHeliyon · 2024Article
- MYO3B promotes cancer progression in endometrial cancer by mediating the calcium ion-RhoA/ROCK1 signaling pathway.Journal of cancer research and clinical oncology · 2024Article
- Trpv6 channel targeting using monoclonal antibody induces prostate cancer cell apoptosis and tumor regression.Cell death & disease · 2024Article
- Review
- Dysregulation of calcium homeostasis in cancer and its role in chemoresistance.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- STAC3 as a poor prognostic biomarker in renal clear cell carcinoma: relationship with immune infiltration.American journal of cancer research · 2024Article
- Evaluation of IP3R3 Gene Silencing Effect on Pyruvate Dehydrogenase (PDH) Enzyme Activity in Breast Cancer Cells with and Without Estrogen Receptor.Advanced biomedical research · 2024Article
- Investigation of Trpa1 and Trpc1 Immunreactivities in Colon Adenocarcinomas.Cancer management and research · 2024Article
- Profiling of Lymphovascular Space Invasion in Cervical Cancer Revealed PI3K/Akt Signaling Pathway Overactivation and Heterogenic Tumor-Immune Microenvironments.Life (Basel, Switzerland) · 2023Article
- Review
54 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer involves defects in the mechanisms underlying cell proliferation, death and migration. Calcium ions are central to these phenomena, serving as major signalling agents with spatial localization, magnitude and temporal characteristics of calcium signals ultimately determining cell's fate. Cellular Ca(2+) signalling is determined by the concerted action of a molecular Ca(2+)-handling toolkit which includes: active energy-dependent Ca(2+) transporters, Ca(2+)-permeable ion channels, Ca(2+)-binding and storage proteins, Ca(2+)-dependent effectors. In cancer, because of mutations, aberrant expression, regulation and/or subcellular targeting of Ca(2+)-handling/transport protein(s) normal relationships among extracellular, cytosolic, endoplasmic reticulum and mitochondrial Ca(2+) concentrations or spatio-temporal patterns of Ca(2+) signalling become distorted. This causes deregulation of Ca(2+)-dependent effectors that control signalling pathways determining cell's behaviour in a way to promote pathophysiological cancer hallmarks such as enhanced proliferation, survival and invasion. Despite the progress in our understanding of Ca(2+) homeostasis remodelling in cancer cells as well as in identification of the key Ca(2+)-transport molecules promoting certain malignant phenotypes, there is still a lot of work to be done to transform fundamental findings and concepts into new Ca(2+) transport-targeting tools for cancer diagnosis and treatment.
Indexed as
Identifiers
What OpenQuestion holds
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.