ArticleWorld journal of gastroenterology2010
Molecular determinants of the antitumor effects of trichostatin A in pancreatic cancer cells.
Article in World journal of gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 10 citations in OpenAlex.
- Pharmacological Properties of Trichostatin A, Focusing on the Anticancer Potential: A Comprehensive Review.Pharmaceuticals (Basel, Switzerland) · 2022Review
- HDAC inhibitors, MS-275 and salermide, potentiates the anticancer effect of EF24 in human pancreatic cancer cells.EXCLI journal · 2016Article
- EGF-Induced Acetylation of Heterogeneous Nuclear Ribonucleoproteins Is Dependent on KRAS Mutational Status in Colorectal Cancer Cells.PloS one · 2015Article
- HLA-G regulators in cancer medicine: an outline of key requirements.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011Review
- The role of K-ras gene mutation in TRAIL-induced apoptosis in pancreatic and lung cancer cell lines.Cancer chemotherapy and pharmacology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo gain molecular insights into the action of the histone deacetylase inhibitor (HDACI) trichostatin-A (TSA) in pancreatic cancer (PC) cells.
methodsThree PC cell lines, BxPC-3, AsPC-1 and CAPAN-1, were treated with various concentrations of TSA for defined periods of time. DNA synthesis was assessed by measuring the incorporation of 5-bromo-2'-deoxyuridine. Gene expression at the level of mRNA was quantified by real-time polymerase chain reaction. Expression and phosphorylation of proteins was monitored by immunoblotting, applying an infrared imaging technology. To study the role of p38 MAP kinase, the specific enzyme inhibitor SB202190 and an inactive control substance, SB202474, were employed.
resultsTSA most efficiently inhibited BrdU incorporation in BxPC-3 cells, while CAPAN-1 cells displayed the lowest and AsPC-1 cells an intermediate sensitivity. The biological response of the cell lines correlated with the increase of histone H3 acetylation after TSA application. In BxPC-3 cells (which are wild-type for KRAS), TSA strongly inhibited phosphorylation of ERK 1/2 and AKT. In contrast, activities of ERK and AKT in AsPC-1 and CAPAN-1 cells (both expressing oncogenic KRAS) were not or were only modestly affected by TSA treatment. In all three cell lines, but most pronounced in BxPC-3 cells, TSA exposure induced an activation of the MAP kinase p38. Inhibition of p38 by SB202190 slightly but significantly diminished the antiproliferative effect of TSA in BxPC-3 cells. Interestingly, only BxPC-3 cells responded to TSA treatment by a significant increase of the mRNA levels of bax, a pro-apoptotic member of the BCL gene family. Finally, in BxPC-3 and AsPC-1 cells, but not in the cell line CAPAN-1, significantly higher levels of the cell cycle inhibitor protein p21(Waf1) were observed after TSA application.
conclusionThe biological effect of TSA in PC cells correlates with the increase of acetyl-H3, p21(Waf1), phospho-p38 and bax levels, and the decrease of phospho-ERK 1/2 and phospho-AKT.
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.