Evidence map›Paper›PMID 30151243›Full record

ArticleSignal transduction and targeted therapy

Novel HDAC5-interacting motifs of Tbx3 are essential for the suppression of E-cadherin expression and for the promotion of metastasis in hepatocellular carcinoma.

Liang Dong, Qi Dong, Ying Chen, Yichen Li, Bao Zhang, Fanghang Zhou, Xiaoming Lyu, George G Chen, Paul Lai, Hsiang-Fu Kung and 1 more

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy. 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
1.8field-weighted citation impact, top 15% 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, 34 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

11 authors at 5 institutions in 2 countries.

Liang Dong *1Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
Qi Dong *1Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
Ying Chen *1Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
Yichen Li1Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
Bao Zhang2School of Public Health and Tropical Medicine, Southern Medical University, 1023 Shatai Road, 510515 Guangzhou, China.
Fanghang Zhou1Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
Xiaoming Lyu1Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
George G Chen3Department of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.
Paul Lai3Department of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.
Hsiang-Fu Kung4Key Laboratory of Tumor Immunopathology, Ministry of Education of China, and Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, 400038 Chongqing, China.
Ming-Liang He1Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China.
City University of Hong Kong · HKChinese University of Hong Kong · CNCity University of Hong Kong, Shenzhen Research Institute · CNSouthern Medical University · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tbx3, a transcriptional repressor, is essential in the organogenesis of vertebrates, stem cell self-renewal and differentiation, and the carcinogenesis of multiple tumor types. However, the mechanism by which Tbx3 participates in the metastasis of hepatocellular carcinoma (HCC) remains largely unknown. In this study, we show that Tbx3 was dramatically upregulated in clinical HCC samples and that elevated expression of Tbx3 promoted cancer progression. To determine the underlying mechanism, systematic glycine scan mutagenesis and deletion assays were performed. We identified two critical motifs,

Identifiers

PMID30151243
PMCPMC6107554
OpenAlexW2888378005

What OpenQuestion holds

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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.