Evidence map›Paper›PMID 24841500›Full record

ArticleInternational journal of oncology2014

Collagen triple helix repeat containing 1 is overexpressed in hepatocellular carcinoma and promotes cell proliferation and motility.

Masahiko Tameda, Kazushi Sugimoto, Katsuya Shiraki, Norihiko Yamamoto, Ryuji Okamoto, Masanobu Usui, Masaaki Ito, Yoshiyuki Takei, Tsutomu Nobori, Takahiro Kojima and 3 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 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
3.0field-weighted citation impact, top 8% 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, 41 citations in OpenAlex.

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  8. Application Potential ofFrontiers in molecular biosciences · 2022
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  11. [Effects of RNA interference of CTHRC1 on proliferation and apoptosis of thyroid papillary cancer TCP-1 cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 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

13 authors at 2 institutions in 1 country.

Masahiko TamedaFirst Department of Internal Medicine, Mie University School of Medicine, Tsu 514-8507, Japan.
Kazushi SugimotoFirst Department of Internal Medicine, Mie University School of Medicine, Tsu 514-8507, Japan.
Katsuya ShirakiFirst Department of Internal Medicine, Mie University School of Medicine, Tsu 514-8507, Japan.
Norihiko YamamotoFirst Department of Internal Medicine, Mie University School of Medicine, Tsu 514-8507, Japan.
Ryuji OkamotoFirst Department of Internal Medicine, Mie University School of Medicine, Tsu 514-8507, Japan.
Masanobu UsuiDepartment of Hepatobiliary Pancreatic and Transplant Surgery, Mie University School of Medicine, Tsu 514-8507, Japan.
Masaaki ItoFirst Department of Internal Medicine, Mie University School of Medicine, Tsu 514-8507, Japan.
Yoshiyuki TakeiDepartment of Gastroenterology and Hepatology, Mie University School of Medicine, Tsu 514-8507, Japan.
Tsutomu NoboriDepartment of Molecular and Laboratory Medicine, Mie University School of Medicine, Tsu 514-8507, Japan.
Takahiro KojimaDepartment of Molecular Biological Oncology, Faculty of Medicine, University of Tsukuba, Tsukuba 305-8575, Japan.
Hideaki SuzukiResearch Division, MCBI, Tsukuba 305-0035, Japan.
Masako UchidaResearch Division, MCBI, Tsukuba 305-0035, Japan.
Kazuhiko UchidaDepartment of Molecular Biological Oncology, Faculty of Medicine, University of Tsukuba, Tsukuba 305-8575, Japan.
Mie University · JPUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although several therapeutic options are available for hepatocellular carcinoma (HCC), the outcome is still very poor. One reason is the complexity of signal transduction in the pathogenesis of HCC. The aim of this study was to identify new HCC-related genes and to investigate the functions of these genes in the pathogenesis and progression of HCC. Whole genomes of 15 surgically resected HCC specimens were examined for copy number alterations with comparative genomic hybridization. Gene expression was compared between HCC and normal liver tissues. The roles of the new genes in the progression of HCC were studied using cultured cell lines. Copy number gain in chromosome 8q was detected in 53% of HCC tissues examined. The gene that coded for collagen triple helix repeat containing 1 (CTHRC1), located at chromosome 8q22.3, was overexpressed in HCC compared with normal or liver cirrhosis tissues and identified as a new HCC-related gene. CTHRC1 deletion with short hairpin RNA significantly reduced proliferation, migration and invasion of HepG2 and Huh7 cells. In addition, mRNA of integrins β-2 and β-3 was downregulated, with deletion of CTHRC1 in these cells. Immunohistochemical staining on resected HCC tissues showing positive staining areas for CTHRC1 was significantly greater in poorly-differentiated HCC compared with well‑differentiated HCC. Moreover, some cases showed strong staining for CTHRC1 in invasive areas of HCC. CTHRC1 has the potential to be a new biomarker for the aggressive HCC, and to be a new therapeutic target in treating HCC.

Indexed as

Cell MovementCell ProliferationAgedBiomarkers, TumorBlotting, WesternCarcinoma, HepatocellularComparative Genomic HybridizationExtracellular Matrix ProteinsFemaleGene DosageHumansImmunohistochemistryLiver NeoplasmsMaleMiddle AgedReal-Time Polymerase Chain ReactionBiomarkers, TumorCTHRC1 protein, humanExtracellular Matrix Proteins

Identifiers

PMID24841500
PMCPMC4091966
OpenAlexW2094072133

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.