Evidence map›Paper›PMID 27041461›Full record

ArticleActa pharmacologica Sinica2016

Activation of p53 contributes to pseudolaric acid B-induced senescence in human lung cancer cells in vitro.

Guo-Dong Yao, Jing Yang, Qiang Li, Ye Zhang, Min Qi, Si-Miao Fan, Toshihiko Hayashi, Shin-Ichi Tashiro, Satoshi Onodera, Takashi Ikejima

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 26 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

10 authors at 4 institutions in 2 countries.

Guo-Dong YaoChina-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang 110016, China.
Jing YangChina-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang 110016, China.
Qiang LiChina-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang 110016, China.
Ye ZhangChina-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang 110016, China.
Min QiTianjin Taiyang Pharmaceutical Co, Ltd, Tianjin 300457, China.
Si-Miao FanTianjin University of Traditional Chinese Medicine, Tianjin 300193, China.
Toshihiko HayashiChina-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang 110016, China.
Shin-Ichi TashiroInstitute for Clinical and Biomedical Sciences, Kyoto 603-8072, Japan.
Satoshi OnoderaDepartment of Clinical and Pharmaceutical Sciences, Showa Pharmaceutical University, Tokyo 194-8543, Japan.
Takashi IkejimaChina-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang 110016, China.
Shenyang Pharmaceutical University · CNResearch Institute for Applied Sciences · JPShowa Pharmaceutical University · JPTianjin University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimPseudolaric acid B (PAB), a diterpene acid isolated from the root bark of Pseudolarix kaempferi Gordon, has shown to exert anti-tumor effects via inducing cell cycle arrest followed by apoptosis in several cancer cell lines. Here we reported that PAB induced a mitotic catastrophe in human lung cancer A549 cells, which resulted in senescence without apoptosis or necrosis.

methodsThree human lung cancer cell lines (A549, H460 and H1299 cells) were examined. Cell growth inhibition was assessed with MTT assay. Cell cycle distribution was determined using a flow cytometer. Cell nuclear morphology was observed under a fluorescence microscope. Senescent cells were detected using SA-β-Gal staining. Apoptotic and senescent protein expression was examined using Western blot analysis. The expression of p53 and p21 in the cells was downregulated by siRNAs.

resultsTreatment with PAB (5-80 μmol/L) inhibited the growth of A549 cells in dose- and time-dependent manners. Prolonged treatment with PAB (20 μmol/L) caused G2/M arrest at day 1 followed by mitotic catastrophe from day 2, which eventually resulted in cell senescence between days 3 and 4 without cell death (apoptosis or necrosis). Knockdown of p53 expression with siRNA significantly suppressed PAB-induced senescence in A549 cells (p53 wild). Furthermore, PAB-induced senescence was also observed in human lung cancer H460 cells (p53 wild), but not in human lung cancer H1299 cells (p53 null).

conclusionThe anti-tumor action of PAB against human lung cancer A549 cells in vitro involves the induction of senescence through activation of the p53 pathway.

Indexed as

ApoptosisCell Cycle CheckpointsCell Line, TumorCell ProliferationCellular SenescenceCyclin-Dependent Kinase Inhibitor p21DiterpenesDose-Response Relationship, DrugHumansRNA, Small InterferingTumor Suppressor Protein p53Cyclin-Dependent Kinase Inhibitor p21Diterpenespseudolaric acid BRNA, Small InterferingTumor Suppressor Protein p53

Identifiers

PMID27041461
PMCPMC4933766
OpenAlexW2340680928

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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.