Evidence map›Paper›PMID 27082306›Full record

ArticleCancer biology & therapy2016

The p38 MAPK inhibitor BIRB796 enhances the antitumor effects of VX680 in cervical cancer.

Xin Jin, Qingqing Mo, Yu Zhang, Yue Gao, Yuan Wu, Jing Li, Xing Hao, Ding Ma, Qinglei Gao, Pingbo Chen

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-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

19 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  6. Review
  7. Functional Roles of JNK and p38 MAPK Signaling in Nasopharyngeal Carcinoma.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Tumor-infiltrating CD8Drug discovery today · 2021
    Review
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  11. Review
  12. 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

10 authors at 2 institutions in 1 country.

Xin Jina Cancer Biology Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Qingqing Moa Cancer Biology Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Yu Zhanga Cancer Biology Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Yue Gaoa Cancer Biology Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Yuan Wua Cancer Biology Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Jing Lia Cancer Biology Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Xing Haoa Cancer Biology Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Ding Maa Cancer Biology Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Qinglei Gaoa Cancer Biology Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Pingbo Chena Cancer Biology Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , Hubei , China.
Tongji Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

VX680 is a potent and selective inhibitor that targets the Aurora kinase family. The p38 mitogen-activated protein kinase (MAPK) regulates a large number of cellular pathways and plays an important role in the regulation of cell survival and apoptosis. This study aimed to evaluate the effect of VX680 on cervical cancer cells and investigate whether the effects on apoptosis are enhanced by the ablation of p38 MAPK activation. The results suggested that VX680 inhibited the proliferation of cervical cancer cells by causing G2/M phase arrest and endoreduplication and that the apoptotic effect was attenuated by the activation of p38 MAPK. However, the addition of BIRB796, which is an important p38 MAPK inhibitor, effectively eliminated the expression of p-p38 and hence significantly enhanced the cell death induced by VX680 in vitro. Further study demonstrated that BIRB796 cooperated with VX680 to suppress cervical cancer cell growth in a mouse xenograft model. Taken together, our results demonstrated that VX680 induced cell cycle arrest and endoreduplication in human cervical cancer cells. Combined treatment with VX680 and BIRB796 synergistically inhibited tumor growth both in vitro and in vivo. Dual blockade of Aurora kinases and p38 MAPK is therefore a promising strategy for cervical cancer treatment.

Indexed as

AnimalsCyclopropanesFemaleHeLa CellsHumansMiceNaphthalenesp38 Mitogen-Activated Protein KinasesPhenylurea CompoundsPiperazinesProtein Kinase InhibitorsPyrazolesPyrimidinesUterine Cervical NeoplasmsXenograft Model Antitumor AssaysCyclopropanesdoramapimodNaphthalenesp38 Mitogen-Activated Protein KinasesPhenylurea CompoundsPiperazinesProtein Kinase InhibitorsPyrazolesPyrimidinestozasertibApoptosisBIRB796cell cyclecervical cancerp38 MAPKVX680

Identifiers

PMID27082306
PMCPMC4910916
OpenAlexW2339040048

What OpenQuestion holds

Textmetadata
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.