Evidence map›Paper›PMID 25180681›Full record

ArticlePloS one2014

CAV1 promotes HCC cell progression and metastasis through Wnt/β-catenin pathway.

Hongxiu Yu, Huali Shen, Yang Zhang, Fan Zhong, Yinkun Liu, Lunxiu Qin, Pengyuan Yang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.9field-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

32 citing papers in PubMed, 51 citations in OpenAlex.

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  15. Effect of differential hypoxia-related gene expression on glioblastoma.The Journal of international medical research · 2021
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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.

Hongxiu YuInstitutes of Biomedical Sciences of Shanghai Medical School, Fudan University, Shanghai, P. R. China.
Huali ShenInstitutes of Biomedical Sciences of Shanghai Medical School, Fudan University, Shanghai, P. R. China.
Yang ZhangInstitutes of Biomedical Sciences of Shanghai Medical School, Fudan University, Shanghai, P. R. China.
Fan ZhongInstitutes of Biomedical Sciences of Shanghai Medical School, Fudan University, Shanghai, P. R. China.
Yinkun LiuInstitutes of Biomedical Sciences of Shanghai Medical School, Fudan University, Shanghai, P. R. China; Zhongshan Hospital, Fudan University, Shanghai, P. R. China.
Lunxiu QinInstitutes of Biomedical Sciences of Shanghai Medical School, Fudan University, Shanghai, P. R. China; Zhongshan Hospital, Fudan University, Shanghai, P. R. China.
Pengyuan YangInstitutes of Biomedical Sciences of Shanghai Medical School, Fudan University, Shanghai, P. R. China; Department of Chemistry, Fudan University, Shanghai, P. R. China.
Shanghai Medical College of Fudan University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Caveolin-1 (CAV1) has significant roles in many primary tumors and metastasis, despite the fact that malignant cells from different cancer types have different profiles of CAV1 expression. There is little information concerning CAV1 expression and role in hepatocellular carcinoma (HCC) progresion and metastasis. The role of CAV1 in HCC progression was explored in this study. We reported that CAV1 was overexpressed in highly invasive HCC cell lines compared with poorly invasive ones. The immunohistochemical staining was obviously stronger in metastatic HCC samples than in the non-metastatic specimens via tissue microarrays. Furthermore, CAV1 overexpression enhanced HCC cell invasiveness in vitro, and promoted tumorigenicity and lung metastasis in vivo. By contrast, CAV1 stable knockdown markedly reduced these malignant behaviors. Importantly, we found that CAV1 could induce EMT process through Wnt/β-catenin pathway to promote HCC metastasis. We also identify MMP-7 as a novel downstream target of CAV1. We have determined that CAV1 acts as a mediator between hyperactive ERK1/2 signaling and regulation of MMP-7 transcription. Together, these studies mechanistically show a previously unrecognized interplay between CAV1, EMT, ERK1/2 and MMP-7 that is likely significant in the progression of HCC toward metastasis.

Indexed as

Disease ProgressionWnt Signaling PathwayAgedAnimalsbeta CateninCarcinoma, HepatocellularCaveolin 1Cell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene Knockdown TechniquesHumansLiver NeoplasmsMalebeta CateninCaveolin 1

Identifiers

PMID25180681
PMCPMC4152279
OpenAlexW1998292400

What OpenQuestion 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 OpenQuestion graph.