Evidence map›Paper›PMID 30940320›Full record

ArticleBMB reports2019

TP53I11 suppresses epithelial-mesenchymal transition and metastasis of breast cancer cells.

Tongqian Xiao, Zhongjuan Xu, Hai Zhang, Junsa Geng, Yong Qiao, Yu Liang, Yanzhen Yu, Qun Dong, Guangli Suo

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.4field-weighted citation impact, top 45% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  8. Pharmaceuticals (Basel, Switzerland) · 2024
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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

9 authors at 5 institutions in 2 countries.

Tongqian XiaoCAS Key Laboratory of Nano-Bio Interface, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Jiangsu 215123; University of Chinese Academy of Sciences, Beijing 100049, China.
Zhongjuan XuCAS Key Laboratory of Nano-Bio Interface, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Jiangsu 215123, China.
Hai ZhangCAS Key Laboratory of Nano-Bio Interface, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Jiangsu 215123, China.
Junsa GengCAS Key Laboratory of Nano-Bio Interface, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Jiangsu 215123, China; University of Science and Technology of China, Anhui 230026, China.
Yong QiaoCAS Key Laboratory of Nano-Bio Interface, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Jiangsu 215123, China.
Yu LiangCAS Key Laboratory of Nano-Bio Interface, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Jiangsu 215123, China; School of Life Sciences, Shanghai University, Shanghai 200444, China.
Yanzhen YuCAS Key Laboratory of Nano-Bio Interface, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Jiangsu 215123, China; University of Science and Technology of China, Anhui 230026, China.
Qun DongTaikang National Pathology Center, TaikangXianlin Drum Tower Hospital, Jiangsu 210046, China.
Guangli SuoCAS Key Laboratory of Nano-Bio Interface, Suzhou Institute of Nano-Tech and Nano-Bionics, Chinese Academy of Sciences, Jiangsu 215123, China.
Chinese Academy of Sciences · CNShanghai University · CNSuzhou Institute of Nano-tech and Nano-bionics · CNUniversity of Chinese Academy of Sciences · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is widely-considered to be a modulating factor of anoikis and cancer metastasis. We found that, in MDA-MB-231 cells, TP53I11 (tumor protein P53 inducible protein 11) suppressed EMT and migration in vitro, and inhibited metastasis in vivo. Our findings showed that hypoxic treatment upregulated the expression of HIF1α, but reduced TP53I11 protein levels and TP53I11 overexpression reduced HIF1α expression under normal culture and hypoxicconditions, and in xenografts of MDA-MB-231 cells. Considering HIF1α is a master regulator of the hypoxic response and that hypoxia is a crucial trigger of cancer metastasis, our study suggests that TP53I11 may suppress EMT and metastasis by reducing HIF1α protein levels in breast cancer cells. [BMB Reports 2019; 52(6): 379-384].

Indexed as

AnimalsBreast NeoplasmsCell HypoxiaCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleHeterograftsHumansHypoxia-Inducible Factor 1, alpha SubunitMiceMice, NudeNeoplasm MetastasisNeoplasm ProteinsHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitNeoplasm ProteinsTP53I11 protein, human

Identifiers

PMID30940320
PMCPMC6605526
OpenAlexW2955759278

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.