Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (675 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
(13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15-hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE; PGA(1) and PGA(2) as well as their 19-hydroxy derivatives are found in many organs and tissues.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: PGA.
Where it fits in the MeSH classification
- Broader topics
- Prostaglandins
Research landscape
PubMed indexes 923 records tagged with the MeSH heading “Prostaglandins A” (counts retrieved 2026-10-31). 25 of them (2.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 725 records.
Reviews account for 46 records (5.0%) and meta-analyses for 4. Randomized controlled trials number 4 (0.4%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 725 |
| 2000-2009 | 137 |
| 2010-2019 | 36 |
| 2020 onward | 25 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 46 | 5.0% |
| Meta-analyses | 4 | 0.4% |
| Randomized controlled trials | 4 | 0.4% |
Method: PubMed query "Prostaglandins A"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Induction of p53-Dependent Apoptosis by Prostaglandin A2 | 2020 | Research article Design not recorded in structured metadata | 29 | cc by PMID 32213959 · DOI · PMC7175137 |
| Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures | 1990 | Research article Design not recorded in structured metadata | 20 | cc by PMID 2310673 · DOI · PMC1971418 |
| PGA1-induced apoptosis involves specific activation of H-Ras and N-Ras in cellular endomembranes | 2016 | Research article Design not recorded in structured metadata | 7 | cc by PMID 27468687 · DOI · PMC4973357 |
Induction of p53-Dependent Apoptosis by Prostaglandin A2 [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Prostaglandin (PG) A2, one of cyclopentenone PGs, is known to induce activation of apoptosis in various cancer cells.
- Closing excerpt
- In contrast to apoptosis in HCT116 cells, PGA2 may induce apoptosis in a fashion of less potency, which is independent of p53 and DNA-PK in HCT116 p53-/- cells.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (315 words)
Prostaglandin (PG) A2, one of cyclopentenone PGs, is known to induce activation of apoptosis in various cancer cells. Although PGA2 has been reported to cause activation of apoptosis by altering the expression of apoptosis-related genes, the role of p53, one of the most critical pro-apoptotic genes, on PGA2-induced apoptosis has not been clarified yet. To address this issue, we compared the apoptosis in HCT116 p53 null cells (HCT116 p53-/-) to that in HCT116 cells containing the wild type p53 gene. Cell death induced by PGA2 was associated with phosphorylation of histone H2A variant H2AX (H2AX), activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase 1 in HCT116 cells. Induction of apoptosis in PGA2-treated cells was almost completely prevented by pretreatment with a pan-caspase inhibitor, z-VAD-Fmk, or an inhibitor of protein synthesis, cycloheximide. While PGA2 induced apoptosis in HCT116 cells, phosphorylation of p53 and transcriptional induction of p53-target genes such as p21WAF1, PUMA, BAX, NOXA, and DR5 occurred. Besides, pretreatment of pifithrin-α (PFT-α), a chemical inhibitor of p53's transcriptional activity, interfered with the induction of apoptosis in PGA2-treated HCT116 cells. Pretreatment of NU7441, a small molecule inhibitor of DNA-activated protein kinase (DNA-PK) suppressed PGA2-induced phosphorylation of p53 and apoptosis as well. Moreover, among target genes of p53, knockdown of DR5 expression by RNA interference, suppressed PGA2-induced apoptosis. In the meanwhile, in HCT116 p53-/- cells, PGA2 induced apoptosis in delayed time points and with less potency. Delayed apoptosis by PGA2 in HCT116 p53-/- cells was also associated with phosphorylation of H2AX but was not inhibited by either PFT- or NU7441. Collectively, these results suggest the following. PGA2 may induce p53-dependent apoptosis in which DNA-PK activates p53, and DR5, a transcriptional target of p53, plays a pivotal role in HCT116 cells. In contrast to apoptosis in HCT116 cells, PGA2 may induce apoptosis in a fashion of less potency, which is independent of p53 and DNA-PK in HCT116 p53-/- cells.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32213959 · DOI · PMC7175137
Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Type A prostaglandins (PGA1 and 16,16-dimethyl-PGA2-methyl ester) were found to block the proliferation of HTLV-I infected cord blood lymphocytes (CBL) in vitro, thus preventing the clonal immortalisation that is considered as a predisposing condition to HTLV-I positive leukaemia.
- Closing excerpt
- These results suggest that the protective effect of PGAs against HTLV-I infection in vitro is mostly related to the direct suppression of the clonal expansion of virus-infected cells, rather than to the anti-viral activity or modulation of the cell-mediated immunity.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (212 words)
Type A prostaglandins (PGA1 and 16,16-dimethyl-PGA2-methyl ester) were found to block the proliferation of HTLV-I infected cord blood lymphocytes (CBL) in vitro, thus preventing the clonal immortalisation that is considered as a predisposing condition to HTLV-I positive leukaemia. PGA1 and di-M-PGA2 did not affect the long-term survival of normal non-infected CBL, whereas they suppressed the proliferation of an established cord-blood derived HTLV-I positive cell line, MT-2. As shown by the number of HTLV-I infected p19+ cells, the block of the selection of immortalised, infected clones by PGAs did not appear to be due to an inhibition of early stages of HTLV-I infection. The possibility that the effect of PGAs could be mediated by an action on the immune response was also examined. PGAs regulated the cell-mediated cytotoxic function of CBL to a different extent when normal non-infected or HTLV-I exposed CBL were compared. In fact, PGAs down-regulated the natural killing and macrophage/lymphocyte cytotoxic response of normal CBL, whereas they did not modify the already depressed immune response of CBL challenged with HTLV-I. These results suggest that the protective effect of PGAs against HTLV-I infection in vitro is mostly related to the direct suppression of the clonal expansion of virus-infected cells, rather than to the anti-viral activity or modulation of the cell-mediated immunity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 2310673 · DOI · PMC1971418
PGA1-induced apoptosis involves specific activation of H-Ras and N-Ras in cellular endomembranes [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The cyclopentenone prostaglandin A1 (PGA1) is an inducer of cell death in cancer cells.
- Closing excerpt
- Our results highlight a novel mechanism that may be of potential interest for tumor treatment.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (148 words)
The cyclopentenone prostaglandin A1 (PGA1) is an inducer of cell death in cancer cells. However, the mechanism that initiates this cytotoxic response remains elusive. Here we report that PGA1 triggers apoptosis by a process that entails the specific activation of H- and N-Ras isoforms, leading to caspase activation. Cells without H- and N-Ras did not undergo apoptosis upon PGA1 treatment; in these cells, the cellular demise was rescued by overexpression of either H-Ras or N-Ras. Consistently, the mutant H-Ras-C118S, defective for binding PGA1, did not produce cell death. Molecular analysis revealed a key role for the RAF-MEK-ERK signaling pathway in the apoptotic process through the induction of calpain activity and caspase-12 cleavage. We propose that PGA1 evokes a specific physiological cell death program, through H- and N-Ras, but not K-Ras, activation at endomembranes. Our results highlight a novel mechanism that may be of potential interest for tumor treatment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27468687 · DOI · PMC4973357
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Role of prostaglandins in the pathogenesis of Bartter's syndrome [4]
- Research article Renal prostaglandins and the regulation of blood pressure and sodium and water homeostasis [5]
- Research article A-class prostaglandins: early findings and new perspectives for overcoming tumor chemoresistance [6]
- Research article Preparation and evaluation of o/w type emulsions containing antitumor prostaglandin [7]
- Research article Ischemic Stroke and Six Genetic Variants in CRP, EPHX2, FGA, and NOTCH3 Genes: A Meta-Analysis [8]
- Research article Clavulones and related tert-hydroxycyclopentenone fatty acids: occurrence, physiological activity and problem of biogenetic origin [9]
References
- Lee SB, Lee S, Park JY, Lee SY, Kim HS. Induction of p53-Dependent Apoptosis by Prostaglandin A2. . 2020. PMID 32213959 · DOI · PMC7175137
- D'Onofrio C, Alvino E, Garaci E, Bonmassar E, Santoro MG. Selection of HTLV-I positive clones is prevented by prostaglandin A in infected cord blood cultures. . 1990. PMID 2310673 · DOI · PMC1971418
- Anta B, Pérez-Rodríguez A, Castro J, García-Domínguez CA, Ibiza S, Martínez N, et al.. PGA1-induced apoptosis involves specific activation of H-Ras and N-Ras in cellular endomembranes. . 2016. PMID 27468687 · DOI · PMC4973357
- Fichman MP, Telfer N, Zia P, Speckart P, Golub M, Rude R. Role of prostaglandins in the pathogenesis of Bartter's syndrome. Am J Med. 1976. PMID 798488 · DOI
- Lee JB, Patak RV, Mookerjee BK. Renal prostaglandins and the regulation of blood pressure and sodium and water homeostasis. Am J Med. 1976. PMID 798489 · DOI
- Díez-Dacal B, Pérez-Sala D. A-class prostaglandins: early findings and new perspectives for overcoming tumor chemoresistance. Cancer Lett. 2012. PMID 22407242 · DOI
- Fukushima S, Kishimoto S, Takeuchi Y, Fukushima M. Preparation and evaluation of o/w type emulsions containing antitumor prostaglandin. Adv Drug Deliv Rev. 2000. PMID 11104898 · DOI
- González-Giraldo Y, Barreto GE, Fava C, Forero DA. Ischemic Stroke and Six Genetic Variants in CRP, EPHX2, FGA, and NOTCH3 Genes: A Meta-Analysis. J Stroke Cerebrovasc Dis. 2016. PMID 27266621 · DOI
- Grechkin AN. Clavulones and related tert-hydroxycyclopentenone fatty acids: occurrence, physiological activity and problem of biogenetic origin. J Lipid Mediat Cell Signal. 1995. PMID 7551677 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.