Evidence map›Paper›PMID 26572558›Full record

ArticleMolecular medicine reports2016

Effects of maslinic acid on the proliferation and apoptosis of A549 lung cancer cells.

Xue Bai, Yi Zhang, Hongfang Jiang, Peng Yang, Hui Li, Yue Zhang, Ping He

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Paeonol inhibits proliferation and induces cell apoptosis of human T24 and 5637 bladder cancer cells in vitro and in vivo.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  8. Review
  9. Article
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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

7 authors at 1 institution in 1 country.

Xue BaiDepartment of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Yi ZhangDepartment of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Hongfang JiangDepartment of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Peng YangDepartment of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Hui LiDepartment of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Yue ZhangDepartment of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
Ping HeDepartment of Geriatrics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maslinic acid (MA) is a pentacyclic triterpene acid that is present in numerous dietary plants. Although certain studies have demonstrated that MA has anti‑cancer properties in different cell types, the effect of MA on lung cancer cell proliferation and apoptosis and the potential underlying mechanisms remain to be elucidated. In the present study, A549 lung cancer cells were treated with different doses of MA and it was found that MA significantly inhibited A549 cell growth in a dose‑dependent manner. In addition, Annexin V/propidium iodide flow cytometric analysis demonstrated that MA induced apoptosis of A549 cells. The present study also confirmed that MA induced apoptosis by observing morphological alterations. In addition, the effect of MA treatment on the levels of apoptosis‑associated proteins was examined. The results demonstrated that MA treatment suppressed the expression of caspase‑3, ‑8 and ‑9, and increased the expression of cleaved caspase‑3, ‑8 and ‑9 in a dose‑dependent manner. The level of inhibitors of apoptosis (IAPs) and Smac, which are possible upstream factors of caspase proteins, were also examined. It was found that MA treatment increased the protein expression of Smac and decreased the protein levels of c‑IAP1, c‑IAP2, X‑linked inhibitor of apoptosis protein (XIAP) and Survivin in a dose‑dependent manner. These results suggested that MA inhibited proliferation and induced apoptosis of A549 cells through regulation of caspase cleavage as well as Smac, c-IAP1, c-IAP2, XIAP and Survivin.

Indexed as

ApoptosisCell Line, TumorCell ProliferationCell ShapeGene Expression Regulation, NeoplasticHumansOleanolic AcidTriterpenesmaslinic acidOleanolic AcidTriterpenes

Identifiers

PMID26572558
PMCPMC4686082
OpenAlexW2099347347

What OpenQuestion holds

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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.