ArticleNeoplasia (New York, N.Y.)2012
CLCA2 as a p53-inducible senescence mediator.
Article in Neoplasia (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
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Who cites it
27 citing papers in PubMed.
- Dissecting cross-lineage tumourigenesis under p53 inactivation through single-cell multi-omics and spatial transcriptomics.Clinical and translational medicine · 2025Article
- Robust p53 phenotypes and prospective downstream targets in telomerase-immortalized human cells.Oncotarget · 2025Article
- Adeno-associated virus-mediated intraprostatic suppression ofGenes & diseases · 2024Article
- TP63 truncating mutation causes increased cell apoptosis and premature ovarian insufficiency by enhanced transcriptional activation of CLCA2.Journal of ovarian research · 2024Article
- CLCA2: A Potential Guardian against Premature Senescence and Skin Aging.Biomedicines · 2024Article
- Gene Expression Analysis of a Topical Serum Comprised of Plant-based Adaptogens Developed to Support Homeostasis and Skin Quality.The Journal of clinical and aesthetic dermatology · 2024Article
- Transcriptomic changes during the replicative senescence of human articular chondrocytes.bioRxiv : the preprint server for biology · 2023Article
- Review
- Article
- The calcium-activated chloride channel-associated protein rCLCA2 is expressed throughout rat epidermis, facilitates apoptosis and is downmodulated by UVB.Histochemistry and cell biology · 2021Article
- Molecular mapping of interstitial lung disease reveals a phenotypically distinct senescent basal epithelial cell population.JCI insight · 2021Article
- Microenvironment Stiffness Amplifies Post-ischemia Heart Regeneration in Response to Exogenous Extracellular Matrix Proteins in Neonatal Mice.Frontiers in cardiovascular medicine · 2021Article
- Prognostic value of chloride channel accessory mRNA expression in colon cancer.Oncology letters · 2019Article
- Emerging roles for multifunctional ion channel auxiliary subunits in cancer.Cell calcium · 2019Review
- Article
- CLCA4 inhibits bladder cancer cell proliferation, migration, and invasion by suppressing the PI3K/AKT pathway.Oncotarget · 2017Article
- EPSIN 3, A Novel p53 Target, Regulates the Apoptotic Pathway and Gastric Carcinogenesis.Neoplasia (New York, N.Y.) · 2017Article
- Article
- Article
- Late Cornified Envelope Group I, a novel target of p53, regulates PRMT5 activity.Neoplasia (New York, N.Y.) · 2014Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53 is a tumor suppressor gene that is frequently mutated in multiple cancer tissues. Activated p53 protein regulates its downstream genes and subsequently inhibits malignant transformation by inducing cell cycle arrest, apoptosis, DNA repair, and senescence. However, genes involved in the p53-mediated senescence pathway are not yet fully elucidated. Through the screening of two genome-wide expression profile data sets, one for cells in which exogenous p53 was introduced and the other for senescent fibroblasts, we have identified chloride channel accessory 2 (CLCA2) as a p53-inducible senescence-associated gene. CLCA2 was remarkably induced by replicative senescence as well as oxidative stress in a p53-dependent manner. We also found that ectopically expressed CLCA2 induced cellular senescence, and the down-regulation of CLCA2 by small interfering RNA caused inhibition of oxidative stress-induced senescence. Interestingly, the reduced expression of CLCA2 was frequently observed in various kinds of cancers including prostate cancer, whereas its expression was not affected in precancerous prostatic intraepithelial neoplasia. Thus, our findings suggest a crucial role of p53/CLCA2-mediated senescence induction as a barrier for malignant transformation.
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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.