Evidence map›Paper›PMID 25749036›Full record

ArticleOncotarget2015

FBXW7 suppresses epithelial-mesenchymal transition, stemness and metastatic potential of cholangiocarcinoma cells.

Hui Yang, Xiaofei Lu, Ziming Liu, Lili Chen, Yunfei Xu, Yuli Wang, Guangwei Wei, Yuxin Chen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
10.3field-weighted citation impact, top 1% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025
    Review
  8. Article
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  10. Transcriptional Up-Regulation of FBXW7 by KInternational journal of molecular sciences · 2024
    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

8 authors at 4 institutions in 1 country.

Hui YangDepartment of Hepatobiliary Surgery, Qilu Hospital of Shandong University, Jinan, China.
Xiaofei LuDepartment of Hepatobiliary Surgery, Qilu Hospital of Shandong University, Jinan, China.
Ziming LiuDepartment of Emergency Medicine, Jinan Fifth People's Hospital, Jinan, China.
Lili ChenDepartment of Pathology, Jinan Fourth People's Hospital, Jinan, China.
Yunfei XuDepartment of Hepatobiliary Surgery, Qilu Hospital of Shandong University, Jinan, China.
Yuli WangDepartment of Anatomy and Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University School of Medicine, Jinan, China.
Guangwei WeiDepartment of Anatomy and Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University School of Medicine, Jinan, China.
Yuxin ChenDepartment of Hepatobiliary Surgery, Qilu Hospital of Shandong University, Jinan, China.
Qilu Hospital of Shandong University · CNShandong University · CNFourth People’s Hospital of Jinan · CNShandong First Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) plays a fundamental role in cancer metastasis. The ubiquitin ligase FBXW7, a general tumor suppressor in human cancer, has been implicated in diverse cellular processes, however, its role in cholangiocarcinoma (CCA) metastasis has not been identified. Here, we report a crucial role of FBXW7 in CCA metastasis by regulating EMT. Loss of FBXW7 expression was detected in CCA cells and clinical specimens. Clinicopathological analysis revealed a close correlation between FBXW7 deficiency and metastasis, TNM stage and differentiation in intrahepatic CCA and perihilar CCA. Moreover, FBXW7 silencing in CCA cells dramatically promoted EMT, stem-like capacity and metastasis both in vitro and in vivo. Conversely, FBXW7 overexpression attenuated these processes. Mechanistically, treatment with rapamycin, a mTOR inhibitor, inhibited EMT, stem-like capacity and metastasis induced by FBXW7 silencing both in vitro and in vivo. Furthermore, the expression of EMT regulating transcription factors, snail, slug and ZEB1, were also decreased markedly with rapamycin treatment. In addition, silencing ZEB1 inhibited EMT and metastasis of both CCA cells and FBXW7 deficient CCA cells, which implicated the potential role of ZEB1 in FBXW7/mTOR signaling pathway related CCA metastasis. In conclusion, our findings defined a pivotal function of FBXW7 in CCA metastasis by regulating EMT.

Indexed as

AnimalsBile Duct NeoplasmsCell Cycle ProteinsCell Line, TumorCholangiocarcinomaEpithelial-Mesenchymal TransitionF-Box ProteinsF-Box-WD Repeat-Containing Protein 7HeterograftsHumansMaleMiceMice, NudeNeoplasm MetastasisNeoplastic Stem CellsSignal TransductionCell Cycle ProteinsF-Box ProteinsF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanUbiquitin-Protein LigasesmetastasismTORtumor suppressorubiquitin ligaseZEB1

Identifiers

PMID25749036
PMCPMC4467439
OpenAlexW1579561590

What OpenQuestion holds

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LicenceCC BY
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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.