Evidence map›Paper›PMID 28514765›Full record

ArticleOncotarget2017

BMX/Etk promotes cell proliferation and tumorigenicity of cervical cancer cells through PI3K/AKT/mTOR and STAT3 pathways.

Yuanyuan Li, Nan Cui, Peng-Sheng Zheng, Wen-Ting Yang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Targeting the BMX in cancer: molecular mechanisms and emerging therapeutic strategies.Journal of enzyme inhibition and medicinal chemistry · 2026
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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

4 authors at 2 institutions in 1 country.

Yuanyuan LiDepartment of Reproductive Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.
Nan CuiDepartment of Reproductive Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.
Peng-Sheng ZhengDepartment of Reproductive Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.
Wen-Ting YangDepartment of Reproductive Medicine, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.
First Affiliated Hospital of Xi'an Jiaotong University · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow X-linked kinase (BMX, also known as Etk) has been reported to be involved in cell proliferation, differentiation, apoptosis, migration and invasion in several types of tumors, but its role in cervical carcinoma remains poorly understood. In this study, we showed that BMX expression exhibits a gradually increasing trend from normal cervical tissue to cervical cancer in situ and then to invasive cervical cancer tissue. Through BMX-IN-1, a potent and irreversible BMX kinase inhibitor, inhibited the expression of BMX, the cell proliferation was significantly decreased. Knockdown of BMX in HeLa and SiHa cervical cancer cell lines using two different silencing technologies, TALEN and shRNA, inhibited cell growth in vitro and suppressed xenograft tumor formation in vivo, whereas overexpression of BMX in the cell line C-33A significantly increased cell proliferation. Furthermore, a mechanism study showed that silencing BMX blocked cell cycle transit from G0/G1 to S or G2/M phase, and knockdown of BMX inhibited the expression of p-AKT and p-STAT3. These results suggested that BMX can promote cell proliferation through PI3K/AKT/mTOR and STAT3 signaling pathways in cervical cancer cells.

Indexed as

Signal TransductionAnimalsCell CycleCell Line, TumorCell ProliferationCell Transformation, NeoplasticCervix UteriDisease Models, AnimalFemaleGene Expression RegulationHeterograftsHumansMiceModels, BiologicalPhosphatidylinositol 3-KinasesProtein-Tyrosine KinasesBMX protein, humanPhosphatidylinositol 3-KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKTBMXcell proliferationcervical carcinomaSTAT3

Identifiers

PMID28514765
PMCPMC5564764
OpenAlexW2607736489

What OpenQuestion holds

Textmetadata
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.