Evidence map›Paper›PMID 26420065›Full record

ArticleNature communications2015

PBX3 is targeted by multiple miRNAs and is essential for liver tumour-initiating cells.

Haibo Han, Yantao Du, Wei Zhao, Sheng Li, Dongji Chen, Jing Zhang, Jiang Liu, Zhenhe Suo, Xiuwu Bian, Baocai Xing and 1 more

Erratum issuedOpen access · goldAbstract read
PubMed Publisher
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

47 citing papers in PubMed, 101 citations in OpenAlex.

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  9. The regulation of PBXs and their emerging role in cancer.Journal of cellular and molecular medicine · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 2 countries.

Haibo HanDepartment of Cell Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Center for Molecular and Translational Medicine, Peking University Cancer Hospital and Institute, 52 Fucheng Road, Beijing 100142, China.
Yantao DuDepartment of Cell Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Center for Molecular and Translational Medicine, Peking University Cancer Hospital and Institute, 52 Fucheng Road, Beijing 100142, China.
Wei ZhaoDepartment of Cell Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Center for Molecular and Translational Medicine, Peking University Cancer Hospital and Institute, 52 Fucheng Road, Beijing 100142, China.
Sheng LiDepartment of Cell Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Center for Molecular and Translational Medicine, Peking University Cancer Hospital and Institute, 52 Fucheng Road, Beijing 100142, China.
Dongji ChenDepartment of Cell Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Center for Molecular and Translational Medicine, Peking University Cancer Hospital and Institute, 52 Fucheng Road, Beijing 100142, China.
Jing ZhangBeijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China.
Jiang LiuBeijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100101, China.
Zhenhe SuoDepartment of Pathology, Oslo University Hospital, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo 0379, Norway.
Xiuwu BianInstitute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
Baocai XingDepartment of Hepatobiliary Surgery I, Peking University Cancer Hospital and Institute, Beijing 100142, China.
Zhiqian ZhangDepartment of Cell Biology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Center for Molecular and Translational Medicine, Peking University Cancer Hospital and Institute, 52 Fucheng Road, Beijing 100142, China.
Peking University · CNPeking University Cancer Hospital · CNBeijing Institute of Genomics · CNOslo University Hospital · NOSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumour-initiating cells (TICs) are advocated to constitute the sustaining force to maintain and renew fully established malignancy; however, the molecular mechanisms responsible for these properties are elusive. We previously demonstrated that voltage-gated calcium channel α2δ1 subunit marks hepatocellular carcinoma (HCC) TICs. Here we confirm directly that α2δ1 is a HCC TIC surface marker, and identify let-7c, miR-200b, miR-222 and miR-424 as suppressors of α2δ1(+) HCC TICs. Interestingly, all the four miRNAs synergistically target PBX3, which is sufficient and necessary for the acquisition and maintenance of TIC properties. Moreover, PBX3 drives an essential transcriptional programme, activating the expression of genes critical for HCC TIC stemness including CACNA2D1, EpCAM, SOX2 and NOTCH3. In addition, the expression of CACNA2D1 and PBX3 mRNA is predictive of poor prognosis for HCC patients. Collectively, our study identifies an essential signalling pathway that controls the switch of HCC TIC phenotypes.

Indexed as

ApoptosisCalcium ChannelsCell Line, TumorCell ProliferationFemaleHomeodomain ProteinsHumansLiverLiver NeoplasmsMaleMicroRNAsMiddle AgedNeoplastic Stem CellsProto-Oncogene ProteinsCACNA2D1 protein, humanCalcium ChannelsHomeodomain ProteinsMicroRNAsMIR222, humanMIRN200 microRNA, humanMIRN424 microrna, humanmirnlet7 microRNA, humanproto-oncogene protein Pbx3Proto-Oncogene Proteins

Identifiers

PMID26420065
OpenAlexW2408110481

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.