Evidence map›Paper›PMID 32438569›Full record

ArticleMarine drugs2020

Astaxanthin Modulates Apoptotic Molecules to Induce Death of SKBR3 Breast Cancer Cells.

Min Sung Kim, Yong Tae Ahn, Chul Won Lee, Hyungwoo Kim, Won Gun An

Open access · goldAbstract read
In one paragraph

Article in Marine drugs, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 41 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Min Sung KimDivision of Pharmacology, School of Korean Medicine, Pusan National University, Yangsan 50612, Korea.
Yong Tae AhnResearch Institute for Korean Medicine, Pusan National University, Yangsan 50612, Korea.
Chul Won LeeResearch Institute for Korean Medicine, Pusan National University, Yangsan 50612, Korea.
Hyungwoo KimDivision of Pharmacology, School of Korean Medicine, Pusan National University, Yangsan 50612, Korea.
Won Gun AnDivision of Pharmacology, School of Korean Medicine, Pusan National University, Yangsan 50612, Korea.
Pusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Astaxanthin (AST) is related to apoptosis but the details of the mechanism of how AST makes apoptosis is not clear. The present study investigated apoptotic effects of AST to SKBR3, a breast cancer cell line in detail. Cell viability assay showed cellular proliferation and morphological changes of the cells were observed under AST treatment. FACS analysis indicated that AST blocked cell cycle progression at G0/G1, suppressed proliferation dose-dependently, and induced apoptosis of the cells. The apoptosis of the cells by AST was further demonstrated through the decreased expression level of mutp53 and cleaved a PARP-1 fragment, respectively. In addition, AST induced the intrinsic apoptosis of the cells by activation of Bax/Bcl2, cleaved caspase-3, and cleaved caspase-9 as well as the phosphorylation of ERK1/2, JNK, and p38. Furthermore, AST decreased production of intracellular reactive oxygen species as well as modulated expressions of superoxide dismutases and Pontin, an anti-apoptotic factor. Co-immunoprecipitation assay revealed AST reduced interaction between Pontin and mutant p53. Taken together, these studies proved that AST regulates the expression of apoptotic molecules to induce intrinsic apoptosis of the cells, suggesting AST therapy might provide an alternative for improving the efficacies of other anti-cancer therapies for breast cancer.

Indexed as

Antineoplastic AgentsApoptosisBreast NeoplasmsCell Line, TumorCell SurvivalFemaleHumansp38 Mitogen-Activated Protein KinasesXanthophyllsAntineoplastic Agentsastaxanthinep38 Mitogen-Activated Protein KinasesXanthophyllsapoptosisastaxanthinBax/Bcl2MAPKmutp53PARP-1PontinROSSKBR3SOD

Identifiers

PMID32438569
PMCPMC7281348
OpenAlexW3028211195

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.