Evidence map›Paper›PMID 25593641›Full record

ArticleBiomolecules & therapeutics2015

The Histone Deacetylase Inhibitor Trichostatin A Sensitizes Human Renal Carcinoma Cells to TRAIL-Induced Apoptosis through Down-Regulation of c-FLIPL.

Min Ho Han, Cheol Park, Taek Kyu Kwon, Gi-Young Kim, Wun-Jae Kim, Sang Hoon Hong, Young Hyun Yoo, Yung Hyun Choi

Open access · greenAbstract read
In one paragraph

Article in Biomolecules & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Trichostatin A potentiates TRAIL-induced antitumor effects via inhibition of ERK/FOXM1 pathway in gastric cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  9. Article
  10. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

Min Ho HanDepartment of Biochemistry, College of Oriental Medicine, Dong-Eui University, Busan 614-851.
Cheol ParkDepartment of Molecular Biology, College of Natural Sciences, Dongeui University, Busan 614-714.
Taek Kyu KwonDepartment of Immunology, School of Medicine, Keimyung University, Daegu 704-701.
Gi-Young KimLaboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, Jeju 690-756.
Wun-Jae KimDepartment of Urology, College of Medicine, Chungbuk National University, Cheongju 362-763.
Sang Hoon HongDepartment of Internal Medicine, College of Oriental Medicine, Dong-Eui University, Busan 614-851.
Young Hyun YooDepartment of Anatomy and Cell Biology, Dong-A University College of Medicine and Mitochondria Hub Regulation Center, Busan 602-714.
Yung Hyun ChoiDepartment of Biochemistry, College of Oriental Medicine, Dong-Eui University, Busan 614-851 ; Anti-Aging Research Center & Blue-BioIndustry RIC, Dongeui University, Busan 614-714, Republic of Korea.
Dong-Eui University · KRChungbuk National University · KRDong-A University · KRJeju National University · KRKeimyung University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone acetylation plays a critical role in the regulation of transcription by altering the structure of chromatin, and it may influence the resistance of some tumor cells to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) by regulating the gene expression of components of the TRAIL signaling pathway. In this study, we investigated the effects and molecular mechanisms of trichostatin A (TSA), a histone deacetylase inhibitor, in sensitizing TRAIL-induced apoptosis in Caki human renal carcinoma cells. Our results indicate that nontoxic concentrations of TSA substantially enhance TRAIL-induced apoptosis compared with treatment with either agent alone. Cotreatment with TSA and TRAIL effectively induced cleavage of Bid and loss of mitochondrial membrane potential (MMP), which was associated with the activation of caspases (-3, -8, and -9) and degradation of poly (ADP-ribose) polymerase (PARP), contributing toward the sensitization to TRAIL. Combined treatment with TSA and TRAIL significantly reduced the levels of the cellular Fas-associated death domain (FADD)-like interleukin-1β-converting enzyme (FLICE) inhibitory protein (c-FLIP), whereas those of death receptor (DR) 4, DR5, and FADD remained unchanged. The synergistic effect of TAS and TRAIL was perfectly attenuated in c-FLIPL-overexpressing Caki cells. Taken together, the present study demonstrates that down-regulation of c-FLIP contributes to TSA-facilitated TRAIL-induced apoptosis, amplifying the death receptor, as well as mitochondria-mediated apoptotic signaling pathways.

Indexed as

Apoptosisc-FLIPLTRAILTrichostatin A

Identifiers

PMID25593641
PMCPMC4286747
OpenAlexW2006331115

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Registered trials

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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.