Evidence map›Paper›PMID 26130968›Full record

ArticleCancer cell international2015

The dual PI3K/mTOR inhibitor NVP-BEZ235 inhibits proliferation and induces apoptosis of burkitt lymphoma cells.

Chuntuan Li, Pengliang Xin, Huifang Xiao, Yan Zheng, Yuanling Huang, Xiongpeng Zhu

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-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

13 citing papers in PubMed, 25 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

6 authors at 1 institution in 1 country.

Chuntuan LiDepartment of Haematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000 Fujian Province China.
Pengliang XinDepartment of Haematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000 Fujian Province China.
Huifang XiaoDepartment of Haematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000 Fujian Province China.
Yan ZhengDepartment of Haematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000 Fujian Province China.
Yuanling HuangDepartment of Haematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000 Fujian Province China.
Xiongpeng ZhuDepartment of Haematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000 Fujian Province China.
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPhosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway is a therapy target of cancer. We aimed to confirm the effect of dual PI3K/mTOR inhibitor NVP-BEZ235 on cell proliferation and apoptosis in Burkitt lymphoma (BL) cells.

methodsTwo human BL cell lines, CA46 and RAJI were used in this study. The proliferation of BL cells was detected by manganese tricarbonyl transfer (MTT) assay. Cell cycle and apoptosis assay were examined by flow cytometric analysis. The phosphorylation levels of AKT (Thr308), AKT (Ser473), and RPS6 were evaluated by western blot analysis.

resultsNVP-BEZ235 significantly inhibited the proliferation of BL cells (CA46 and RAJI) and the inhibition effect was time and dose-dependent. Cell cycle analysis indicated that the cells (CA46 and RAJI) were mostly arrested in G1/G0 phase. Cell apoptosis assay showed that the late apoptotic cells were significantly increased after 72 h treatment by 100 nmol/L of NVP-BEZ235. In addition, results also found that NVP-BEZ235 reduced the phosphorylation levels of AKT (Thr308), AKT (Ser473), and PRS6 in BL cells (CA46 and RAJI). Moreover, this inhibition effect on phosphorylation was dose-dependent.

conclusionsNVP-BEZ235 effectively inhibited cell proliferation by G0/G1 cell-cycle arrest and induced apoptosis through deregulating PI3K/Akt/mTOR pathway in BL cells.

Indexed as

ApoptosisBurkitt lymphomaCell proliferationNVP-BEZ235Phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin pathway

Identifiers

PMID26130968
PMCPMC4486138
OpenAlexW1581950988

What OpenQuestion holds

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LicenceCC BY
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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.