ArticleOncogene2014
H-Ras-driven tumoral maintenance is sustained through caveolin-1-dependent alterations in calcium signaling.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Association of Caveolin-1 Expression With Prostate Cancer: A Systematic Review and Meta-Analysis.Frontiers in oncology · 2020Pooled it
- Iron and Other Metal Ions in Human Health and Disease.MedComm · 2026Review
- Caveolin-1 Stabilizes SERCA2 to Counteract Acute Kidney Injury via Suppression of CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The importance of mitochondria and mitochondrial calcium signaling in health and disease: an updated outlook on inflammation.Journal of translational medicine · 2026Review
- The role of mitochondria-endoplasmic reticulum crosstalk in colorectal cancer.Genes & diseases · 2026Review
- Thermodynamic Considerations on the Biophysical Interaction between Low-Energy Electromagnetic Fields and Biosystems.Membranes · 2024Article
- The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells.International journal of molecular sciences · 2022Review
- Molecular mechanisms and consequences of mitochondrial permeability transition.Nature reviews. Molecular cell biology · 2022Review
- Article
- Mitochondrial Control of Genomic Instability in Cancer.Cancers · 2021Review
- The MAMs Structure and Its Role in Cell Death.Cells · 2021Review
- Tracking changes in adaptation to suspension growth for MDCK cells: cell growth correlates with levels of metabolites, enzymes and proteins.Applied microbiology and biotechnology · 2021Article
- Review
- Various Aspects of Calcium Signaling in the Regulation of Apoptosis, Autophagy, Cell Proliferation, and Cancer.International journal of molecular sciences · 2020Review
- Mitochondrial Metabolism, Contact Sites and Cellular Calcium Signaling: Implications for Tumorigenesis.Cancers · 2020Review
- Review
- Caveolin-1 suppresses tumor formation through the inhibition of the unfolded protein response.Cell death & disease · 2020Article
- Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology.Biomolecules · 2020Review
- Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer.Cancer metastasis reviews · 2020Review
- TOB1 suppresses proliferation in K-Ras wild-type pancreatic cancer.Cancer medicine · 2020Article
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 1 institution in 1 country.
Funding
Abstract
A growing body of research has highlighted the complex range of tumoral traits acquired during H-Ras-driven transformation and maintenance, which include proliferative signaling, growth suppressor evasion and resistance to cell death. Clear molecular information about these processes is not yet available, but recent evidence has provided solid support for the importance of mitochondria. Here, we show that the induction of oncogenic H-Ras leads to changes in intracellular calcium (Ca(2+)), evaluate the temporal relationship between oncogene expression and mitochondrial physiology, and demonstrate that Ca(2+) homeostasis is altered by caveolin-1, a protein that has a key role in tumor maintenance. Our results indicate that tumor-suppressor caveolin-1 is a core component of the Ca(2+)-dependent apoptotic pathway and participates in the regulation of critical mitochondrial functions during tumor development. The compromised caveolin-1/Ca(2+) axis contributes to failure in both mitochondrial metabolism and apoptosis, thereby sustaining the neoplastic phenotype. These results illustrate a direct link between Ca(2+) regulation and mitochondrial biology in cancer.
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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.