Evidence map›Paper›PMID 28716136›Full record

ArticleJournal of experimental & clinical cancer research : CR2017

Up-regulation of CDK16 by multiple mechanisms in hepatocellular carcinoma promotes tumor progression.

Yitao Wang, Xian Qin, Tao Guo, Pengpeng Liu, Ping Wu, Zhisu Liu

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Yitao WangDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Xian QinDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Tao GuoDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Pengpeng LiuDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Ping WuDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Zhisu LiuDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China. whdxlzs2005@163.com.
Zhongnan Hospital of Wuhan University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) remains difficult to cure due to lack of effective treatment and the molecular mechanisms are complex and not completely understood. In this study, We investigated the role of CDK16 in tumor progression of HCC.

methodsWe interrogated the expression level of CDK16 by polymerase chain reaction and immunohistochemistry(IHC) and studied its clinical significance. The functional role of CDK16 on HCC was studied via gain and loss of function in vitro and in vivo. Luciferase reporter assay and Chromatin immunoprecipitation(ChIP) assay were performed to investigate the transcriptional and post-transcriptional mechanisms involved in the regulation of CDK16.

resultsCDK16 expression was significantly up-regulated in HCC and higher expression of CDK16 was positively correlated with aggressive clinicopathological phenotype and poorer survival rates. Functionally, knockdown of CDK16 suppressed proliferation in vitro and in vivo. Inactivation of CDK16 also induced apoptosis and cell cycle arrest. Most importantly, CDK16 promoted epithelial mesenchymal transition and tumor invasion by activating β-catenin signaling. In addition, We identified E2F1 as a positive transcriptional regulator of CDK16. Moreover, down regulation of miR-125b-5p enhanced CDK16 expression at post-transcriptional level.

conclusionWe provided the first evidence that CDK16 is an bona fide oncogene in HCC, and multiple activating mechanisms at transcriptional and posttranscriptional levels together contributes to CDK16 up-regulation in HCC.

Indexed as

AgedAnimalsCarcinoma, HepatocellularCell Line, TumorCyclin-Dependent KinasesDisease ProgressionFemaleHumansLiver NeoplasmsMaleMiceMice, Inbred BALB CMice, NudePrognosisTransfectionUp-RegulationCyclin-Dependent KinasesPCTAIRE-1 protein kinaseCyclin dependent Kinase 16 (CDK16)E2F1 transcription factorEpithelial mesenchymal transition (EMT)Hepatocellular carcinoma (HCC)miR-125b-5p

Identifiers

PMID28716136
PMCPMC5514535
OpenAlexW3008014253

What Socratic 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 Socratic graph.