Evidence map›Paper›PMID 28489585›Full record

ArticleOncotarget2017

POU2F1 over-expression correlates with poor prognoses and promotes cell growth and epithelial-to-mesenchymal transition in hepatocellular carcinoma.

Yonghao Zhong, Hongyang Huang, Min Chen, Jinzhou Huang, Qingxia Wu, Guang-Rong Yan, De Chen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 34 citations in OpenAlex.

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  16. DLX6-AS1/miR-204-5p/OCT1 positive feedback loop promotes tumor progression and epithelial-mesenchymal transition in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 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

7 authors at 2 institutions in 1 country.

Yonghao ZhongBiomedicine Research Center, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Hongyang HuangBiomedicine Research Center, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Min ChenBiomedicine Research Center, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Jinzhou HuangBiomedicine Research Center, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Qingxia WuBiomedicine Research Center, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Guang-Rong YanBiomedicine Research Center, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
De ChenBiomedicine Research Center, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Guangzhou Medical University · CNThird Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite recent efforts to understand activities of POU domain class 2 transcription factor 1 (POU2F1), little is known about the roles of POU2F1 in hepatocellular carcinoma (HCC) tumorigenesis and its correlation with any clinicopathological feature of HCC. In this study, we found that POU2F1 was significantly up-regulated in HCC specimens compared with adjacent non-cancerous liver specimens. The high POU2F1 protein expression level positively correlated with large tumor size, high histological grade, tumor metastasis and advanced clinical stage, and HCC patients with high POU2F1 levels exhibited poor prognoses. We further demonstrated that POU2F1 over-expression promoted HCC cell proliferation, colony formation, epithelial-to-mesenchymal transition (EMT), migration and invasion, while silencing of POU2F1 inhibited these malignant phenotypes. POU2F1 induced the expression of Twist1, Snai1, Snai2 and ZEB1 genes which are involved in the regulation of EMT. Furthermore, POU2F1 was up-regulated by AKT pathway in HCC, and POU2F1 over-expression reversed the inhibition of malignant phenotypes induced by AKT knock-down, indicating POU2F1 is a key down-stream effector of AKT pathway. Collectively, our results indicate that POU2F1 over-expression is positively associated with aggressive phenotypes and poor survival in patients with HCC, and POU2F1 regulated by AKT pathway promotes HCC aggressive phenotypes by regulating the transcription of EMT genes. POU2F1 may be employed as a new prognostic factor and therapeutic target for HCC.

Indexed as

Gene ExpressionAdultAgedCarcinoma, HepatocellularCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene SilencingHumansLiver NeoplasmsMaleMiddle AgedNeoplasm GradingNeoplasm MetastasisOctamer Transcription Factor-1Octamer Transcription Factor-1POU2F1 protein, humanProto-Oncogene Proteins c-akthepatocellular carcinomaPOU2F1

Identifiers

PMID28489585
PMCPMC5546464
OpenAlexW2607467556

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.