ArticleProceedings of the National Academy of Sciences of the United States of America2009
Intramitochondrial calcium regulation by the FHIT gene product sensitizes to apoptosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 3 of them syntheses 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
33 citing papers in PubMed, 3 syntheses or guidelines pooled it, 65 citations in OpenAlex.
- The clinicopathological significance of FHIT hypermethylation in non-small cell lung cancer, a meta-analysis and literature review.Scientific reports · 2016Pooled it
- The clinicopathological significance and ethnic difference of FHIT hypermethylation in non-small-cell lung carcinoma: a meta-analysis and literature review.Drug design, development and therapy · 2016Pooled it
- The clinicopathological significance and drug target potential of FHIT in breast cancer, a meta-analysis and literature review.Drug design, development and therapy · 2015Pooled it
- Integrative bioinformatics analysis for identifying the mitochondrial-related gene associated with immune infiltration in sarcopenia.Medicine · 2025Article
- Integrated analysis ofCell cycle (Georgetown, Tex.) · 2024Review
- CircFhit Modulates GABAergic Synaptic Transmission via Regulating the Parental Gene Fhit Expression in the Spinal Dorsal Horn in a Rat Model of Neuropathic Pain.Neuroscience bulletin · 2023Article
- Review
- Review
- Mitochondrial calcium uniporter complex modulation in cancerogenesis.Cell cycle (Georgetown, Tex.) · 2019Review
- Fhit-Fdxr interaction in the mitochondria: modulation of reactive oxygen species generation and apoptosis in cancer cells.Cell death & disease · 2019Article
- The Influence of MicroRNAs on Mitochondrial Calcium.Frontiers in physiology · 2018Review
- Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases.International review of cell and molecular biology · 2018Review
- Lipids at membrane contact sites: cell signaling and ion transport.EMBO reports · 2017Review
- Regulation of Endoplasmic Reticulum-Mitochondria CaFrontiers in oncology · 2017Review
- Endoplasmic Reticulum-Mitochondrial CaFrontiers in oncology · 2017Review
- Tumor Suppressor Genes within Common Fragile Sites Are Active Players in the DNA Damage Response.PLoS genetics · 2016Review
- Intravital imaging reveals p53-dependent cancer cell death induced by phototherapy via calcium signaling.Oncotarget · 2015Article
- p53 and Ca(2+) signaling from the endoplasmic reticulum: partners in anti-cancer therapies.Oncoscience · 2015Article
- Mitochondrial Ca(2+) Remodeling is a Prime Factor in Oncogenic Behavior.Frontiers in oncology · 2015Review
- The FHIT gene product: tumor suppressor and genome "caretaker".Cellular and molecular life sciences : CMLS · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Despite the growing interest in the Fhit tumor suppressor protein, frequently deleted in human cancers, the mechanism of its powerful proapoptotic activity has remained elusive. We here demonstrate that Fhit sensitizes the low-affinity Ca(2+) transporters of mitochondria, enhancing Ca(2+) uptake into the organelle both in intact and in permabilized cells, and potentiating the effect of apoptotic agents. This effect can be attributed to the fraction of Fhit sorted to mitochondria, as a fully mitochondrial Fhit (a chimeric protein including a mitochondrial targeting sequence) retains the Ca(2+) signaling properties of Fhit and the proapoptotic activity of the native protein (whereas the effects on the cell cycle are lost). Thus, the partial sorting of Fhit to mitochondria allows to finely tune the sensitivity of the organelle to the highly pleiomorphic Ca(2+) signals, synergizing with apoptotic challenges. This concept, and the identification of the molecular machinery, may provide ways to act on apoptotic cell death and its derangement in cancer.
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.