Evidence map›Paper›PMID 26296979›Full record

ArticleOncotarget2015

Positive feedback loop of hepatoma-derived growth factor and β-catenin promotes carcinogenesis of colorectal cancer.

Jiayan Lian, Jianming Tang, Huijuan Shi, Hui Li, Tiantian Zhen, Wenlin Xie, Fenfen Zhang, Yang Yang, Anjia Han

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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
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  4. MicroRNA-939 Directly TargetsOncoTargets and therapy · 2020
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  12. The clinicopathological significance of ZNF10 in invasive ductal carcinoma of the breast.International journal of clinical and experimental pathology · 2018
    Article
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  16. Review
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

9 authors at 2 institutions in 1 country.

Jiayan LianDepartment of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
Jianming TangDepartment of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
Huijuan ShiDepartment of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
Hui LiDepartment of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
Tiantian ZhenDepartment of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
Wenlin XieDepartment of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
Fenfen ZhangDepartment of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
Yang YangDepartment of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
Anjia HanDepartment of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
The First Affiliated Hospital, Sun Yat-sen University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To clarify the role of hepatoma-derived growth factor (HDGF) and β-catenin in carcinogenesis of colorectal cancer (CRC), our results showed that high HDGF expression was found in CRC cells and tissues and significantly related to histological differentiation (p = 0.035) and lymph node metastasis (p = 0.000). Significant positive correlation between HDGF expression and β-catenin abnormal expression was found in CRC tissues. High HDGF and lymph node metastasis were the strong independent prognostic indicators for reduced overall survival in CRC patients. HDGF knockdown dramatically inhibited cellular proliferation, migration, invasion, and tumorigenesis, both in vitro and in vivo, but induced G1 phase arrest and apoptosis in CRC cells. HDGF knock-down dramatically suppressed β-catenin and its down-stream genes expression in CRC cells. Intriguingly, β-catenin knock-down dramatically suppressed HDGF expression in CRC cells. Human recombinant Wnt3a and DKK1 treatment increased and decreased HDGF, β-catenin, c-Myc, cyclin D1, MMP9, and phos-GSK-3β (Ser9) protein expression in nuclear and cytoplasmic fraction of CRC cells upon β-catenin knock-down, respectively. Three HDGF-binding elements in β-catenin promoter were found and specific for transcriptional activation of β-catenin in CRC cells. In conclusion, our results first suggest that HDGF and β-catenin interacts as a positive feedback loop, which plays an important role in carcinogenesis and progression of CRC.

Indexed as

AnimalsApoptosisbeta CateninBinding SitesBiomarkers, TumorCarcinogenesisCell MovementCell ProliferationColorectal NeoplasmsDisease ProgressionFeedback, PhysiologicalFemaleG1 Phase Cell Cycle CheckpointsHCT116 CellsHT29 CellsHumansbeta CateninBiomarkers, TumorCTNNB1 protein, humanhepatoma-derived growth factorIntercellular Signaling Peptides and Proteinscolorectal cancerhepatoma-derived growth factorβ-catenin

Identifiers

PMID26296979
PMCPMC4745732
OpenAlexW1901170167

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.