EMILIN2 down-modulates the Wnt signalling pathway and suppresses breast cancer cell growth and migration

2014 ◽  
Vol 232 (4) ◽  
pp. 391-404 ◽  
Author(s):  
Stefano Marastoni ◽  
Eva Andreuzzi ◽  
Alice Paulitti ◽  
Roberta Colladel ◽  
Rosanna Pellicani ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Wnt Signalling ◽  
Signalling Pathway ◽  
Cancer Cell Growth ◽  
Cell Growth And Migration ◽  
Breast Cancer Cell Growth ◽  
And Migration

scholarly journals p66α Suppresses Breast Cancer Cell Growth and Migration by Acting as Co-Activator of p53

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3593
Author(s):  
Qun Zhang ◽  
Yihong Zhang ◽  
Jie Zhang ◽  
Dan Zhang ◽  
Mengying Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Tumor Suppressor ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Target Genes ◽  
Cancer Cell Growth ◽  
Cell Growth And Migration ◽  
Breast Cancer Cell Growth ◽  
And Migration

p66α is a GATA zinc finger domain-containing transcription factor that has been shown to be essential for gene silencing by participating in the NuRD complex. Several studies have suggested that p66α is a risk gene for a wide spectrum of diseases such as diabetes, schizophrenia, and breast cancer; however, its biological role has not been defined. Here, we report that p66α functions as a tumor suppressor to inhibit breast cancer cell growth and migration, evidenced by the fact that the depletion of p66α results in accelerated tumor growth and migration of breast cancer cells. Mechanistically, immunoprecipitation assays identify p66α as a p53-interacting protein that binds the DNA-binding domain of p53 molecule predominantly via its CR2 domain. Depletion of p66α in multiple breast cells results in decreased expression of p53 target genes, while over-expression of p66α results in increased expression of these target genes. Moreover, p66α promotes the transactivity of p53 by enhancing p53 binding at target promoters. Together, these findings demonstrate that p66α is a tumor suppressor by functioning as a co-activator of p53.

scholarly journals Aspirin Modifies Inflammatory Mediators and Metabolomic Profiles and Contributes to the Suppression of Obesity-Associated Breast Cancer Cell Growth

2020 ◽  
Vol 21 (13) ◽  
pp. 4652 ◽  
Author(s):  
Chia-Chien Hsieh ◽  
Huai-Hsuan Chiu ◽  
Chih-Hsuan Wang ◽  
Ching-Hua Kuo
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Fatty Acid ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Growth ◽  
Cell Growth And Migration ◽  
Breast Cancer Cell Growth ◽  
And Migration

Breast cancer is the most common cancer among women. Adiposity generally accompanies immune cell infiltration and cytokine secretion, which is ideal for tumor development. Aspirin is a chemopreventive agent against several types of cancer. The aim of this study was to investigate whether aspirin inhibits the growth of 4T1 breast cancer cells by inhibiting the inflammatory response and regulating the metabolomic profile of 3T3-L1 adipocytes. 3T3-L1 adipocyte-conditioned medium (Ad-CM) was used to mimic the obese adipose tissue microenvironment in 4T1 cells. The results revealed that aspirin inhibited macrophage chemoattractant protein (MCP-1), interleukin (IL-6), IL-1β, and plasminogen activator inhibitor (PAI-1) production in 3T3-L1 adipocytes stimulated by tumor necrosis factor-alpha (TNF-α) and lipopolysaccharide (LPS). In the obesity-associated model, Ad-CM significantly promoted 4T1 cell growth and migration, which were attenuated after aspirin treatment. The results of metabolic analyses using Ad-CM showed that amino acid metabolites and oxidative stress were increased in mature 3T3-L1 adipocytes compared to those in fibroblasts. Aspirin treatment modified metabolites involved in suppressing lipogenesis, oxidative stress, and neoplastic formation. In the relative fatty acid quantitation analysis of Ad-CM, aspirin diminished fatty acid contents of C16:1, C18:1, C18:2, C20:4, and C24:1. This study is the first to show that aspirin modifies the metabolomics and fatty acid composition of 3T3-L1 adipocytes and inhibits obesity-associated inflammation that contributes to obesity-related breast cancer cell growth and migration.

Abstract 5540: CCN5/WISP-2 prevents leptin-induced breast cancer cell growth and migration

2011 ◽  
Author(s):  
Inamul Haque ◽  
Snigdha Banerjee ◽  
Kakali Dhar ◽  
Indranil Chattopadhyay ◽  
Amitabha Ray ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Growth ◽  
Cell Growth And Migration ◽  
Breast Cancer Cell Growth ◽  
And Migration

Abstract 3131: IGF-I regulates Cyr61-induced breast cancer cell growth and migration

2010 ◽  
Author(s):  
Suren Sarkissyan ◽  
Marianna Sarkissyan ◽  
Yanyuan Wu ◽  
H Phillip Koeffler ◽  
Jaydutt V. Vadgama
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Growth ◽  
Cell Growth And Migration ◽  
Breast Cancer Cell Growth ◽  
Igf I ◽  
And Migration

scholarly journals Ecust004 Suppresses Breast Cancer Cell Growth, Invasion, and Migration via EMT Regulation

2021 ◽  
Vol Volume 15 ◽  
pp. 3451-3461
Author(s):  
Ziyu Liu ◽  
Leilei Huang ◽  
Liwei Sun ◽  
Hui Nie ◽  
Yuqi Liang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Growth ◽  
Invasion And Migration ◽  
Breast Cancer Cell Growth ◽  
And Migration
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