Evidence map›Paper›PMID 27103891›Full record

ArticleEXCLI journal2015

Trans-1,3-diphenyl-2,3-epoxypropan-1-one, a chalcone derivative, induces apoptosis via ROS-mediated down-regulation of Bcl-xL in human leukemia HL-60 cells.

Eun-Yi Ko, Seung-Hong Lee, Ji-Yeon Ko, Jeong Yong Moon, Weon-Jong Yoon, Ginnae Ahn, Seong Woon Roh, Kichul Cho, You-Jin Jeon, Daekyung Kim and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EXCLI journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 85% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

11 authors at 5 institutions in 1 country.

Eun-Yi KoJeju Center, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea; School of Marine Biomedical Sciences, Jeju National University, Jeju 690-756, Republic of Korea.
Seung-Hong LeeDivision of Food Bioscience, Konkuk University, Chungju Chungbuk 380-701, Republic of Korea.
Ji-Yeon KoSchool of Marine Biomedical Sciences, Jeju National University, Jeju 690-756, Republic of Korea.
Jeong Yong MoonSubtropical Horticulture Research Institute, Jeju National University, Jeju 690-756, Republic of Korea.
Weon-Jong YoonJeju Biodiversity Research Institute, Jeju Technopark, Jeju, 699-943, Republic of Korea.
Ginnae AhnDepartment of Marine Bio-Food Sciences, Chonnam National University, Yeosu 550-749, Republic of Korea.
Seong Woon RohJeju Center, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea.
Kichul ChoJeju Center, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea.
You-Jin JeonSchool of Marine Biomedical Sciences, Jeju National University, Jeju 690-756, Republic of Korea.
Daekyung KimJeju Center, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea.
Kil-Nam KimJeju Center, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea; Department of Marin Biotechnology, University of Science and Technology, Daejeon 305-350, Republic of Korea.
Jeju National University · KRKorea Basic Science Institute · KRChonnam National University · KRJeju TechnoPark · KRKonkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The anticancer effects of trans-1,3-diphenyl-2,3-epoxypropan-1-one (DPEP), a chalcone derivative, were investigated in human leukemia HL-60 cells. Treatment of HL-60 cells with various concentration of DPEP resulted in a sequence of events characteristic of apoptosis, including loss of cell viability, morphological changes, and increased sub-G1 DNA content. We demonstrated that DPEP elevates reactive oxygen species (ROS) levels in HL-60 cells, and that the ROS scavenger N-acetylcysteine (NAC) could block DPEP-induced ROS generation and apoptosis. Western blot analysis revealed that DPEP inhibits Bcl-xL expression, leading to caspase-3 activation and poly-ADP-ribose polymerase (PARP) cleavage, thereby inducing apoptosis. However, NAC pre-treatment significantly inhibited the activation of caspase-3 and PARP cleavage and reduced Bcl-xL levels. These findings provide the first evidence that DPEP may inhibit the growth of HL-60 cells and induce apoptosis through a ROS-mediated Bcl-xL pathway.

Indexed as

anticancerapoptosisBcl-xLreactive oxygen species (ROS)trans-1,3-diphenyl-2,3-epoxypropan-1-one (DPEP)

Identifiers

PMID27103891
PMCPMC4834817
OpenAlexW2414255595

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.