ArticleOncotarget2015
The endoplasmic reticulum mitochondrial calcium cross talk is downregulated in malignant pleural mesothelioma cells and plays a critical role in apoptosis inhibition.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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
20 citing papers in PubMed, 31 citations in OpenAlex.
- Damage-Associated Molecular Patterns in Mesothelioma: Drivers of Inflammation and Therapeutic Targets.International journal of molecular sciences · 2026Review
- Failed metabolic adaptation to stress contributes to epidermal cell adhesion defects in Darier disease.Science advances · 2026Article
- Proliferation of pleural mesothelioma cells is enhanced by the microRNA-197-3p activity.Frontiers in oncology · 2026Article
- FABP5 is a key player in metabolic modulation and NF-κB dependent inflammation driving pleural mesothelioma.Communications biology · 2025Article
- Reduced ER-mitochondria connectivity promotes neuroblastoma multidrug resistance.The EMBO journal · 2022Article
- Mitochondria: Insights into Crucial Features to Overcome Cancer Chemoresistance.International journal of molecular sciences · 2021Review
- Various Aspects of Calcium Signaling in the Regulation of Apoptosis, Autophagy, Cell Proliferation, and Cancer.International journal of molecular sciences · 2020Review
- Metformin Induces Apoptosis and Inhibits Notch1 in Malignant Pleural Mesothelioma Cells.Frontiers in cell and developmental biology · 2020Article
- Targeting Calcium Signalling in Malignant Mesothelioma.Cancers · 2019Review
- The Protective Role of Calbindin-DInternational journal of molecular sciences · 2019Article
- Mitochondrial CaFEBS letters · 2019Review
- STAT3 localizes to the ER, acting as a gatekeeper for ER-mitochondrion CaCell death and differentiation · 2019Article
- Pannexin 2 Localizes at ER-Mitochondria Contact Sites.Cancers · 2019Article
- Article
- Heterogeneous Contributing Factors in MPM Disease Development and Progression: Biological Advances and Clinical Implications.International journal of molecular sciences · 2018Review
- New Perspectives on Diagnosis and Therapy of Malignant Pleural Mesothelioma.Frontiers in oncology · 2018Review
- MicroRNA-138 and MicroRNA-25 Down-regulate Mitochondrial Calcium Uniporter, Causing the Pulmonary Arterial Hypertension Cancer Phenotype.American journal of respiratory and critical care medicine · 2017Article
- KCa1.1, a calcium-activated potassium channel subunit alpha 1, is targeted by miR-17-5p and modulates cell migration in malignant pleural mesothelioma.Molecular cancer · 2016Article
- Mcl-1 involvement in mitochondrial dynamics is associated with apoptotic cell death.Molecular biology of the cell · 2016Article
- Overexpression or absence of calretinin in mouse primary mesothelial cells inversely affects proliferation and cell migration.Respiratory research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The failure of apoptosis may contribute to the formation of cancer and to its resistance to therapy. Malignant pleural mesothelioma (MPM) is an aggressive tumor that responds poorly to standard chemo- and radio-therapies. Several studies have demonstrated that a plethora of oncogenes and tumor suppressors contribute to MPM onset/progression. Importantly, most of these genes are involved in the regulation of calcium (Ca2+)-handling. Cellular Ca2+ signaling is an important regulator of many physiological processes, and it has been widely reported to participate in the regulation of apoptotic cell death in cancer cells and tissues. However, in MPM the role of cellular Ca2+ has been poorly investigated. Therefore, we examined whether Ca2+ is involved in MPM. We found that mesothelioma cell lines and short-term cultures obtained from MPM-affected patients exhibited a critical dysregulation in Ca2+ signaling. We determined that this characteristic was associated with resistance to apoptotic stimuli and that correction of intracellular Ca2+ signaling resulted in the rescue of efficient apoptotic responses. In addition, we discovered that mitochondrial Ca2+-uptake plays a pivotal role as an inducer of apoptosis in MPM. Altogether, these findings suggest the identification of new MPM markers, which in turn could be potential targets for new therapeutic approaches.
Indexed as
Identifiers
What Socratic 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 Socratic graph.