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

Gain of oncogenic function of p53 mutants induces invasive phenotypes in human breast cancer cells by silencing CCN5/WISP-2.

Cancer research - 15 Jun 2008

Dhar Gopal, Banerjee Snigdha, Dhar Kakali, Tawfik Ossama, Mayo Matthew S, Vanveldhuizen Peter J, Banerjee Sushanta K

Abstract excerpt

CCN5/WISP-2 is overexpressed in noninvasive breast cancer cells and tissue samples, whereas its expression is minimal or undetected in invasive conditions. CCN5/WISP-2 has been considered as an antiinvasive gene because CCN5/WISP-2 silencing augments the invasive phenotypes in vitro. However, the...

Read the complete abstract on PubMed

Topics

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

Share to Carcinoma, Intraductal, Noninfiltrating
Share to Cell Movement
Share to Chloramphenicol O-Acetyltransferase

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Intercellular Signaling Peptides and Proteins

Share to Neoplasm Invasiveness

Share to Receptors, Estrogen

Share to Repressor Proteins

Share to RNA Interference

Source

Identifiers

PMID: 18559502
DOI: 10.1158/0008-5472.CAN-08-0316

Genes

CCN5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-18559502-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Gain of oncogenic function of p53 mutants induces invasive phenotypes in human breast cancer cells by silencing CCN5/WISP-2.PMID 18559502Read ↗

Role of WISP-2/CCN5 in the maintenance of a differentiated and noninvasive phenotype in human breast cancer cells.Semantic proximity Read ↗

Deficiency of CCN5/WISP-2-Driven Program in breast cancer Promotes Cancer Epithelial cells to mesenchymal stem cells and Breast Cancer growthSemantic proximity Read ↗

Loss of WISP2/CCN5 in estrogen-dependent MCF7 human breast cancer cells promotes a stem-like cell phenotype.Semantic proximity Read ↗

CCN6 (WISP3) as a new regulator of the epithelial phenotype in breast cancer.Semantic proximity Read ↗

Suppression of Tumorigenicity 5 Ameliorates Tumor Characteristics of Invasive Breast Cancer Cells via Integrating ERK/JNK PathwaySemantic proximity Read ↗

The WISP1/Src/MIF Axis Promotes the Malignant Phenotype of Non-Invasive Breast Cancer CellsSemantic proximity Read ↗

The WISP1/Src/MIF Axis Promotes the Malignant Phenotype of Non-Invasive MCF7 Breast Cancer Cells.Semantic proximity Read ↗

WISP-1/CCN4 regulates osteogenesis by enhancing BMP-2 activity.Semantic proximity Read ↗

WIP and WICH/WIRE co-ordinately control invadopodium formation and maturation in human breast cancer cell invasionSemantic proximity Read ↗

The effects of shRNA-mediated gene silencing of transcription factor SNAI1 on the biological phenotypes of breast cancer cell line MCF-7.Semantic proximity Read ↗

CSN5 Isopeptidase Activity Links COP9 Signalosome Activation to Breast Cancer ProgressionSemantic proximity Read ↗

Tissue microarray analysis of maspin expression and its reverse correlation with mutant p53 in various tumors.Semantic proximity Read ↗

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