Evidence map›Paper›PMID 28560058›Full record

ArticleAmerican journal of cancer research2017

Flot2 promotes tumor growth and metastasis through modulating cell cycle and inducing epithelial-mesenchymal transition of hepatocellular carcinoma.

Cheng-Hao Wang, Xiao-Dong Zhu, De-Ning Ma, Hui-Chuan Sun, Dong-Mei Gao, Ning Zhang, Cheng-Dong Qin, Yuan-Yuan Zhang, Bo-Gen Ye, Hao Cai and 3 more

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

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  16. Flotillin membrane domains in cancer.Cancer metastasis reviews · 2020
    Review
  17. Article
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  19. Copy number variations ofTranslational cancer research · 2020
    Article
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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

13 authors at 2 institutions in 2 countries.

Cheng-Hao WangLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
Xiao-Dong ZhuLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
De-Ning MaLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
Hui-Chuan SunLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
Dong-Mei GaoLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
Ning ZhangDepartment of Liver Surgery, Fudan University Shanghai Cancer Center, Cancer HospitalShanghai 200032, China.
Cheng-Dong QinLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
Yuan-Yuan ZhangLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
Bo-Gen YeLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
Hao CaiLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
Wen-Kai ShiLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
Man-Qin CaoLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
Zhao-You TangLiver Cancer Institute, Zhongshan Hospital, Fudan UniversityShanghai 200032, China.
Fudan University · CNFudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Flotillin-2 (Flot2) is a highly conserved and ubiquitously expressed protein that resides on the cytoplasmic side of the cell membrane within specific cholesterol rich microdomains. Some studies have reported that overexpression of Flot2 is related to cancer progression. However, the role of Flot2 in hepatocellular carcinoma (HCC) remains unclarified. In this study, we aim to explore the correlation between Flot2 expression and HCC progression and the underlying mechanism. In the present study, overexpression of Flot2 in HCC tissues and cell lines was detected, and forced overexpression of Flot2 significantly promoted the proliferation, migration, invasion and metastasis of HCC in vitro and in vivo by modulating cell cycle and inducing EMT, which was mediated via up-regulation of Twist as a result of Raf/MEK/ERK1/2 pathway activation. In contrast, silencing Flot2 expression inhibited these biological processes. Furthermore, high expression of Flot2 was significantly correlated with poor prognosis of HCC patients after curative resection and is an independent risk factor. In conclusion, Flot2 promoted tumor growth and metastasis of HCC through modulating cell cycle and inducing EMT. The expression of Flot2 may play a key role in HCC progression and may be regarded as a potential poor prognostic marker for HCC.

Indexed as

cell cycleEMTFlot2Hepatocellular carcinomametastasis

Identifiers

PMID28560058
PMCPMC5446475
OpenAlexW2987031765

What OpenQuestion holds

Textmetadata
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.