Evidence map›Paper›PMID 25490748›Full record

ArticlePloS one2014

Mimulone-induced autophagy through p53-mediated AMPK/mTOR pathway increases caspase-mediated apoptotic cell death in A549 human lung cancer cells.

Hyun-Kyu An, Kyoung-Sook Kim, Ji-Won Lee, Mi-Hyun Park, Hyung-In Moon, Shin-Ji Park, Ji-Sue Baik, Cheorl-Ho Kim, Young-Choon Lee

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 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.

Hyun-Kyu AnCollege of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.
Kyoung-Sook KimCollege of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.
Ji-Won LeeCollege of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.
Mi-Hyun ParkCollege of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.
Hyung-In MoonCollege of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.
Shin-Ji ParkCollege of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.
Ji-Sue BaikCollege of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.
Cheorl-Ho KimMolecular and Cellular Glycobiology Unit, Department of Biological Sciences, SungKyunKwan University, Kyunggi-Do, 440-746, South Korea.
Young-Choon LeeCollege of Natural Resources and Life Science, Dong-A University, Busan, 604-714, South Korea.
Dong-A University · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anticancer properties and mechanisms of mimulone (MML), C-geranylflavonoid isolated from the Paulownia tomentosa fruits, were firstly elucidated in this study. MML prevented cell proliferation in a dose- and time-dependent way and triggered apoptosis through the extrinsic pathway in A549 human lung adenocarcinoma cells. Furthermore, MML-treated cells displayed autophagic features, such as the formation of autophagic vacuoles, a primary morphological feature of autophagy, and the accumulation of microtubule-associated protein 1 light chain 3 (LC3) puncta, another typical maker of autophagy, as determined by FITC-conjugated immunostaining and monodansylcadaverine (MDC) staining, respectively. The expression levels of LC3-I and LC3-II, specific markers of autophagy, were also augmented by MML treatment. Autophagy inhibition by 3-methyladenine (3-MA), pharmacological autophagy inhibitor, and shRNA knockdown of Beclin-1 reduced apoptotic cell death induced by MML. Autophagic flux was not significantly affected by MML treatment and lysosomal inhibitor, chloroquine (CQ) suppressed MML-induced autophagy and apoptosis. MML-induced autophagy was promoted by decreases in p53 and p-mTOR levels and increase of p-AMPK. Moreover, inhibition of p53 transactivation by pifithrin-α (PFT-α) and knockdown of p53 enhanced induction of autophagy and finally promoted apoptotic cell death. Overall, the results demonstrate that autophagy contributes to the cytotoxicity of MML in cancer cells harboring wild-type p53. This study strongly suggests that MML is a potential candidate for an anticancer agent targeting both autophagy and apoptotic cell death in human lung cancer. Moreover, co-treatment of MML and p53 inhibitor would be more effective in human lung cancer therapy.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAMP-Activated Protein KinasesAntineoplastic Agents, PhytogenicApoptosisAutophagyBenzothiazolesCell Line, TumorCell SurvivalFlavanonesGene Knockdown TechniquesHCT116 CellsHumansLamialesLung NeoplasmsMCF-7 CellsAMP-Activated Protein KinasesAntineoplastic Agents, PhytogenicBenzothiazolesFlavanonesmimuloneMTOR protein, humanpifithrinTolueneTOR Serine-Threonine KinasesTumor Suppressor Protein p53

Identifiers

PMID25490748
PMCPMC4260910
OpenAlexW2022318020

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.