Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The matricellular protein CCN1 suppresses hepatocarcinogenesis by inhibiting compensatory proliferation.

Oncogene - 10 Mar 2016

Chen C-C, Kim K-H, Lau L F

Abstract excerpt

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide, and is on the rise in the United States. Previous studies showed that the matricellular protein CCN1 (CYR61) is induced during hepatic injuries and functions to restrict and resolve liver fibrosis. Here, we show that CCN1 suppresses hepatocarcinogenesis by inhibiting carcinogen-induced compensatory hepatocyte...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Carcinogenesis
Share to Carcinoma, Hepatocellular
Share to Diethylnitrosamine

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to ErbB Receptors

Share to Liver Neoplasms

Share to p38 Mitogen-Activated Protein Kinases

Share to Reactive Oxygen Species

Source

Open in PubMed Open full text

Identifiers

PMID: 26028023
DOI: 10.1038/onc.2015.190
PMCID: PMC4666840

Genes

CCN1
EGFR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 11 closest

The matricellular protein CCN1 suppresses hepatocarcinogenesis by inhibiting compensatory proliferation.PMID 26028023Read ↗

Canopy Homolog 2 contributes to liver oncogenesis by promoting unfolded protein response–dependent destabilization of tumor protein P53Semantic proximity Read ↗

β‐catenin deficiency in hepatocytes aggravates hepatocarcinogenesis driven by oncogenic β‐catenin and METSemantic proximity Read ↗

DJ-1 promotes development of DEN-induced hepatocellular carcinoma and proliferation of liver cancer cells.Semantic proximity Read ↗

Ccne1 Overexpression Causes Chromosome Instability in Liver Cells and Liver Tumor Development in MiceSemantic proximity Read ↗

Nrf1 is endowed with a dominant tumor-repressing effect onto the Wnt/β-Catenin-dependent and -independent signaling networks in the human liver cancerSemantic proximity Read ↗

Small Maf deficiency recapitulates the liver phenotypes of Nrf1- and Nrf2-deficient mice.Semantic proximity Read ↗

Loss of SPTBN1 Suppresses Autophagy Via SETD7-mediated YAP Methylation in Hepatocellular Carcinoma Initiation and DevelopmentSemantic proximity Read ↗

Loss of Dicer1 impairs hepatocyte survival and leads to chronic inflammation and progenitor cell activation.Semantic proximity Read ↗

SOCS1 Deficiency Promotes Hepatocellular Carcinoma via SOCS3-Dependent CDKN1A Induction and NRF2 ActivationSemantic proximity Read ↗

NFκB1 is a suppressor of neutrophil-driven hepatocellular carcinoma.Semantic proximity Read ↗

c-Met recruits ICAM-1 as a coreceptor to compensate for the loss of CD44 in Cd44 null mice.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.