Evidence map›Paper›PMID 32458633›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2020

Ethanol Extract of Hizikia fusiforme Induces Apoptosis in B16F10 Mouse Melanoma Cells through ROS-Dependent Inhibition of the PI3K/Akt Signaling Pathway.

Cheol Park, Hyesook Lee, Hyun Hwangbo, Seon Yeong Ji, Min Yeong Kim, So Young Kim, Su Hyun Hong, Gi-Young Kim, Yung Hyun Choi

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 13 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

9 authors at 2 institutions in 1 country.

Cheol ParkDepartment of Molecular Biology, College of Natural Sciences, Dong-eui University, Busan 47340, Republic of Korea.
Hyesook LeeAnti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
Hyun HwangboAnti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
Seon Yeong JiAnti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
Min Yeong KimAnti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
So Young KimAnti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
Su Hyun HongAnti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.
Gi-Young KimLaboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, Jeju 63243, Republic of Korea.
Yung Hyun ChoiAnti-Aging Research Center, Dong-eui University, Busan 47340, Republic of Korea.ORCID 0000-0002-1454-3124
Dong-Eui University · KRJeju National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious studies have reported that Hizikia fusiforme, an edible brown seaweed, has diverse health-promoting effects; however, evidence for its anti-cancer potential is still lacking. In this study, we examined the effect of ethanol extract of H. fusiforme (EHF) on the proliferation of B16F10 mouse melanoma cells.

methodsAnalyses of cell viability and apoptosis were performed to study the actions of EHF on B16F10 cells. Cellular reactive oxygen species (ROS) and mitochondrial membrane potential (ΔΨm) were measured using a flow cytometer. Western blot analysis was carried out to measure apoptosis and phosphoinositide 3-kinase (PI3K)/Akt signaling related proteins.

resultsEHF treatment significantly decreased B16F10 cell viability, which was associated with induction of apoptosis. EHF activated caspase-8 and caspase-9, which are involved in the initiation of extrinsic and intrinsic apoptosis pathways, respectively, and also increased caspase-3 activity, a typical effect caspase, subsequently leading to poly (ADP-ribose) polymerase cleavage. In addition, EHF destroyed the integrity of mitochondria and increased Bax/Bcl-2 ratio, which contributed to cytosolic release of cytochrome c. EHF further enhanced intracellular levels of ROS and the addition of N-acetyl cysteine (NAC), a ROS inhibitor, significantly diminished EHF-induced mitochondrial dysfunction and growth inhibition. Moreover, EHF inactivated the PI3K/Akt signaling pathway and LY294002, a PI3K/Akt inhibitor, increased the apoptosis-inducing effect of EHF. However, increased apoptosis and reduced cell viability by simultaneous treatment of EHF and LY294002 were significantly attenuated in the presence of NAC.

conclusionThese results indicate that EHF induces apoptosis through activation of extrinsic and intrinsic apoptotic pathways and ROS-dependent inactivation of PI3K/Akt signaling in B16F10 cells.<br />.

Indexed as

AnimalsApoptosisCell ProliferationEthanolMelanoma, ExperimentalMembrane Potential, MitochondrialMicePhaeophyceaePhosphatidylinositol 3-KinasePlant ExtractsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTumor Cells, CulturedEthanolPhosphatidylinositol 3-KinasePlant ExtractsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesApoptosisB16F10 cellsHizikia fusiformePI3K/AktROS

Identifiers

PMID32458633
PMCPMC7541858
OpenAlexW3029714625

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.