Evidence map›Paper›PMID 22408435›Full record

ArticleInternational journal of molecular sciences2012

Bufalin induces lung cancer cell apoptosis via the inhibition of PI3K/Akt pathway.

Zhitu Zhu, Hongzhi Sun, Guangyou Ma, Zhenghua Wang, Enze Li, Yangyang Liu, Yunpeng Liu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 101 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

7 authors at 2 institutions in 1 country.

Zhitu ZhuDepartment of Oncology, the First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China.
Hongzhi SunDepartment of Oncology, the First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China.
Guangyou MaDepartment of Oncology, the First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China.
Zhenghua WangDepartment of Oncology, the First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China.
Enze LiDepartment of Oncology, the First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China.
Yangyang LiuDepartment of Oncology, the First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121001, China.
Yunpeng LiuDepartment of Oncology, the First Affiliated Hospital of Chinese Medical University, Shenyang, Liaoning 120000, China.
Jinzhou Medical University · CNFirst Affiliated Hospital of Liaoning Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bufalin is a class of toxic steroids which could induce the differentiation and apoptosis of leukemia cells, and induce the apoptosis of gastric, colon and breast cancer cells. However, the anti-tumor effects of bufalin have not been demonstrated in lung cancer. In this study we used A549 human lung adenocarcinoma epithelial cell line as the experimental model to evaluate the potential of bufalin in lung cancer chemotherapy. A549 cells were treated with bufalin, then the proliferation was detected by MTT assay and apoptosis was detected by flow cytometry analysis and Giemsa staining. In addition, A549 cells were treated by Akt inhibitor LY294002 in combination with bufalin and the activation of Akt and Caspase-3 as well as the expression levels of Bax, Bcl-2 and livin were examined by Western blot analysis. The results showed that Bufalin inhibited the proliferation of A549 cells and induced the apoptosis of A549 cells in a dose and time dependent manner. Mechanistically, we found that bufalin inhibited the activation of Akt. Moreover, bufalin synergized with Akt inhibitor to induce the apoptosis of A549 cells and this was associated with the upregulation of Bax expression, the downregulation of Bcl-2 and livin expression, and the activation of Caspase-3. In conclusion, our findings demonstrate that bufalin induces lung cancer cell apoptosis via the inhibition of PI3K/Akt pathway and suggest that bufalin is a potential regimen for combined chemotherapy to overcome the resistance of lung cancer cells to chemotherapeutics induced apoptosis.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAntineoplastic AgentsApoptosisBufanolidesCell ProliferationDown-RegulationHumansLung NeoplasmsOncogene Protein v-aktPhosphatidylinositol 3-KinasesSignal TransductionTumor Cells, CulturedAntineoplastic AgentsbufalinBufanolidesOncogene Protein v-aktPhosphatidylinositol 3-KinasesA549 cellsApoptosisbufalinlung cancerPI3K/Akt

Identifiers

PMID22408435
PMCPMC3292004
OpenAlexW2052183335

What OpenQuestion holds

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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.