Evidence map›Paper›PMID 20335658›Full record

ArticleThe Journal of clinical investigation2010

CHD1L promotes hepatocellular carcinoma progression and metastasis in mice and is associated with these processes in human patients.

Leilei Chen, Tim Hon Man Chan, Yun-Fei Yuan, Liang Hu, Jun Huang, Stephanie Ma, Jian Wang, Sui-Sui Dong, Kwan Ho Tang, Dan Xie and 2 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

89 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.

  1. Pooled it
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  5. CHD1L in cancer and beyond: structure, oncogenic functions, and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025
    Review
  6. Article
  7. The validation of new CHD1L inhibitors as a therapeutic strategy for cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024
    Article
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29 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Leilei ChenDepartment of Clinical Oncology, University of Hong Kong, China.
Tim Hon Man Chan
Yun-Fei Yuan
Liang Hu
Jun Huang
Stephanie Ma
Jian Wang
Sui-Sui Dong
Kwan Ho Tang
Dan Xie
Yan Li
Xin-Yuan Guan
University of Hong Kong · HKState Key Laboratory of Oncology in South ChinaChinese University of Hong Kong · CNEastern Hepatobiliary Surgery Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromodomain helicase/ATPase DNA binding protein 1-like gene (CHD1L) is a recently identified oncogene localized at 1q21, a frequently amplified region in hepatocellular carcinoma (HCC). To explore its oncogenic mechanisms, we set out to identify CHD1L-regulated genes using a chromatin immunoprecipitation-based (ChIP-based) cloning strategy in a human HCC cell line. We then further characterized 1 identified gene, ARHGEF9, which encodes a specific guanine nucleotide exchange factor (GEF) for the Rho small GTPase Cdc42. Overexpression of ARHGEF9 was detected in approximately half the human HCC samples analyzed and positively correlated with CHD1L overexpression. In vitro and in vivo functional studies in mice showed that CHD1L contributed to tumor cell migration, invasion, and metastasis by increasing cell motility and inducing filopodia formation and epithelial-mesenchymal transition (EMT) via ARHGEF9-mediated Cdc42 activation. Silencing ARHGEF9 expression by RNAi effectively abolished the invasive and metastatic abilities of CHD1L in mice. Furthermore, investigation of clinical HCC specimens showed that CHD1L and ARHGEF9 were markedly overexpressed in metastatic HCC tissue compared with healthy tissue. Increased expression of CHD1L was often observed at the invasive front of HCC tumors and correlated with venous infiltration, microsatellite tumor nodule formation, and poor disease-free survival. These findings suggest that CHD1L-ARHGEF9-Cdc42-EMT might be a novel pathway involved in HCC progression and metastasis.

Indexed as

AnimalsCarcinoma, Hepatocellularcdc42 GTP-Binding ProteinCell DifferentiationCell Line, TumorCell MovementDisease ProgressionDNA-Binding ProteinsDNA HelicasesEndothelial CellsFemaleGene Expression Regulation, NeoplasticGuanine Nucleotide Exchange FactorsHumansLiver NeoplasmsMaleARHGEF9 protein, humancdc42 GTP-Binding ProteinCHD1L protein, humanDNA-Binding ProteinsDNA HelicasesGuanine Nucleotide Exchange FactorsRho Guanine Nucleotide Exchange Factors

Identifiers

PMID20335658
PMCPMC2846051
OpenAlexW2058258230

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.