Evidence map›Paper›PMID 27057626›Full record

ArticleOncotarget2016

Critical role of DEK and its regulation in tumorigenesis and metastasis of hepatocellular carcinoma.

Le Yu, Xiaobin Huang, Wenfa Zhang, Huakan Zhao, Gang Wu, Fenglin Lv, Lei Shi, Yong Teng

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  3. Clinicopathological insights and prognostic implications of DEK in association with apoptosis-regulating factors in ovarian cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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  11. [Construction of RNA interference (RNAi) lentiviral expression vector of DEK gene and its effect on the biological behavior of liver cancer cells].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020
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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

8 authors at 2 institutions in 1 country.

Le YuSchool of Life Sciences, Chongqing University, Chongqing 400044, PR China.
Xiaobin HuangSchool of Life Sciences, Chongqing University, Chongqing 400044, PR China.
Wenfa ZhangSchool of Life Sciences, Chongqing University, Chongqing 400044, PR China.
Huakan ZhaoSchool of Life Sciences, Chongqing University, Chongqing 400044, PR China.
Gang WuThird Affiliated Hospital, Third Military Medical University, Chongqing 400044, PR China.
Fenglin LvSchool of Life Sciences, Chongqing University, Chongqing 400044, PR China.
Lei ShiSchool of Life Sciences, Chongqing University, Chongqing 400044, PR China.
Yong TengSchool of Life Sciences, Chongqing University, Chongqing 400044, PR China.
Chongqing University · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality globally. Therefore, it is quite essential to identify novel HCC-related molecules for the discovery of new prognostic markers and therapeutic targets. As an oncogene, DEK plays an important role in cell processes and participates in a variety of cellular metabolic functions, and its altered expression is associated with several human malignancies. However, the functional significance of DEK and the involved complex biological events in HCC development and progression are poorly understood. Here, combing the results from clinical specimens and cultured cell lines, we uncover a critical oncogenic role of DEK, which is highly expressed in HCC cells. DEK protein encompasses two isoforms (isoforms 1 and 2) and isoform 1 is the most frequently expressed DEK isoform in HCC cells. DEK depletion by using shRNA inhibited the cell proliferation and migration in vitro and suppressed tumorigenesis and metastasis in mouse models. Consistently, DEK overexpression regardless of which isoform produced the opposite effects. Further studies showed that DEK induced cell proliferation through upregulating cell cycle related CDK signaling, and promoted cell migration and EMT, at least in part, through the repression of β-catenin/E-cadherin axis. Interestingly, isoform 1 induced cell proliferation more efficiently than isoform 2, however, no functional differences existed between these two isoforms in cell migration. Together, our study indicates that DEK expression is required for tumorigenesis and metastasis of HCC, providing molecular insights for DEK-related pathogenesis and a basis for developing new strategies against HCC.

Indexed as

AnimalsCarcinogenesisCarcinoma, HepatocellularCell MovementCell ProliferationChromosomal Proteins, Non-HistoneHeterograftsHumansKaplan-Meier EstimateLiver NeoplasmsMiceMice, NudeNeoplasm InvasivenessOncogene ProteinsPoly-ADP-Ribose Binding ProteinsProtein IsoformsChromosomal Proteins, Non-HistoneDEK protein, humanOncogene ProteinsPoly-ADP-Ribose Binding ProteinsProtein IsoformsDEKHCCisoformmetastasismigration

Identifiers

PMID27057626
PMCPMC5042019
OpenAlexW2340114270

What OpenQuestion holds

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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.