scholarly journals Identification of a novel metastasis inducing lncRNA which suppresses the KAI1/CD82 metastasis suppressor gene and is upregulated in triple-negative breast cancer

Oncotarget ◽  
2017 ◽  
Vol 8 (40) ◽  
pp. 67538-67552 ◽  
Author(s):  
Ronni Aram ◽  
Iris Dotan ◽  
Agnes Hotz-Wagenblatt ◽  
Dan Canaani
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Suppressor Gene ◽  
Metastasis Suppressor ◽  
Metastasis Suppressor Gene

scholarly journals KIBRA (WWC1) Is a Metastasis Suppressor Gene Affected by Chromosome 5q Loss in Triple-Negative Breast Cancer

Cell Reports ◽  
2018 ◽  
Vol 22 (12) ◽  
pp. 3191-3205 ◽  
Author(s):  
Jennifer F. Knight ◽  
Vanessa Y.C. Sung ◽  
Elena Kuzmin ◽  
Amber L. Couzens ◽  
Danielle A. de Verteuil ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Suppressor Gene ◽  
Metastasis Suppressor ◽  
Metastasis Suppressor Gene ◽  
Chromosome 5Q

scholarly journals ROLE OF TUMOUR SUPPRESSOR GENE P53 IN TRIPLE NEGATIVE BREAST CANCER

2017 ◽  
Vol 5 (4.2) ◽  
pp. 4585-4589
Author(s):  
Priya S Patil ◽  
◽  
Jaydeep N Pol ◽  
Ashalata D Patil ◽  
◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor

scholarly journals Genetic Polymorphisms of Metastasis Suppressor Gene NME1 and Breast Cancer Survival

2008 ◽  
Vol 14 (15) ◽  
pp. 4787-4793 ◽  
Author(s):  
Shimian Qu ◽  
Jirong Long ◽  
Qiuyin Cai ◽  
Xiao-Ou Shu ◽  
Hui Cai ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Genetic Polymorphisms ◽  
Cancer Survival ◽  
Suppressor Gene ◽  
Breast Cancer Survival ◽  
Metastasis Suppressor ◽  
Metastasis Suppressor Gene

EcoRI polymorphism of the metastasis-suppressor gene NME1 in Mexican patients with breast cancer

2005 ◽  
Vol 96 (2) ◽  
pp. 159-161 ◽  
Author(s):  
Susan Andrea Gutierrez Rubio ◽  
Silvia Esperanza Flores Martinez ◽  
Jose Sanchez Corona ◽  
Adriana Patricia Mendizabal Ruiz ◽  
Angel Emilio Suarez Rincon ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Suppressor Gene ◽  
Metastasis Suppressor ◽  
Metastasis Suppressor Gene ◽  
Mexican Patients

scholarly journals TIMP-2 suppresses tumor growth and metastasis in murine model of triple-negative breast cancer

2019 ◽  
Vol 41 (3) ◽  
pp. 313-325 ◽  
Author(s):  
David Peeney ◽  
Sandra M Jensen ◽  
Nadia P Castro ◽  
Sarvesh Kumar ◽  
Silvia Noonan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Signaling Pathways ◽  
Triple Negative Breast Cancer ◽  
Primary Tumor ◽  
Epithelial To Mesenchymal Transition ◽  
Triple Negative ◽  
Metastasis Suppressor ◽  
Mesenchymal Transition ◽  
Tumor Growth And Metastasis

Abstract Metastasis is the primary cause of treatment failures and mortality in most cancers. Triple-negative breast cancer (TNBC) is refractory to treatment and rapidly progresses to disseminated disease. We utilized an orthotopic mouse model that molecularly and phenotypically resembles human TNBC to study the effects of exogenous, daily tissue inhibitor of metalloproteinase-2 (TIMP-2) treatment on tumor growth and metastasis. Our results demonstrated that TIMP-2 treatment maximally suppressed primary tumor growth by ~36–50% and pulmonary metastasis by >92%. Immunostaining assays confirmed disruption of the epithelial to mesenchymal transition (EMT) and promotion of vascular integrity in primary tumor tissues. Immunostaining and RNA sequencing analysis of lung tissue lysates from tumor-bearing mice identified significant changes associated with metastatic colony formation. Specifically, TIMP-2 treatment disrupts periostin localization and critical cell-signaling pathways, including canonical Wnt signaling involved in EMT, as well as PI3K signaling, which modulates proliferative and metastatic behavior through p27 phosphorylation/localization. In conclusion, our study provides evidence in support of a role for TIMP-2 in suppression of triple-negative breast cancer growth and metastasis through modulation of the epithelial to mesenchymal transition, vascular normalization, and signaling pathways associated with metastatic outgrowth. Our findings suggest that TIMP-2, a constituent of the extracellular matrix in normal tissues, may have both direct and systemic antitumor and metastasis suppressor effects, suggesting potential utility in the clinical management of breast cancer progression.

scholarly journals Medroxyprogesterone Acetate Elevation of Nm23-H1 Metastasis Suppressor Expression in Hormone Receptor–Negative Breast Cancer

2005 ◽  
Vol 97 (9) ◽  
pp. 632-642 ◽  
Author(s):  
Diane Palmieri ◽  
Douglas O. Halverson ◽  
Taoufik Ouatas ◽  
Christine E. Horak ◽  
Massimiliano Salerno ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Hormone Receptor ◽  
Pulmonary Metastases ◽  
Suppressor Gene ◽  
Metastasis Suppressor ◽  
Metastasis Suppressor Gene ◽  
Breast Cancer Patients ◽  
Human Breast ◽  
Metastatic Colonization

Abstract Background: Reestablishment of metastasis suppressor gene expression may constitute a therapeutic strategy for high-risk breast cancer patients. We previously showed that medroxyprogesterone acetate (MPA), a progestin that has been tested as treatment for advanced breast cancer, elevates expression of the Nm23-H1 metastasis suppressor gene in hormone receptor–negative metastatic human breast carcinoma cell lines in vitro via a glucocorticoid receptor–based mechanism. Here, we tested whether MPA treatment inhibits metastatic colonization of a hormone receptor–negative breast cancer cell line in vivo. Methods: We tested the soft-agar colony-forming efficiency of untransfected MDA-MB-231T human breast carcinoma cells and MDA-MB-231T cells transfected with antisense Nm23-H1 in the presence and absence of MPA. Pharmacokinetic studies were used to establish dose and injection schedules that led to MPA serum levels in mice similar to those achievable in humans. For in vivo studies, nude mice were injected intravenously with MDA-MB-231T cells. After 4 weeks, mice were randomized to control or MPA arms. Endpoints included incidence, number, and size of gross pulmonary metastases; Nm23-H1 protein expression in gross metastases; and side effects. All statistical tests were two-sided. Results: MPA reduced colony formation of MDA-MB-231T cells by 40%–50% but had no effect on colony formation of Nm23-H1 antisense transfectants. Metastases developed in 100% (95% confidence interval [CI] = 78% to 100% and 77% to 100%, respectively) of control mice injected with MDA-MB-231T cells. In two independent experiments, only 73% (95% CI = 45% to 92%) and 64% (95% CI = 35% to 87%) of mice injected with 2 mg of MPA developed metastases. Mice injected with 2 mg of MPA showed reductions in the mean numbers, per mouse, of all metastases and of large (>3 mm) metastases ( P = .04 and .013, respectively). Nm23-H1 was expressed at high levels in 43% of pulmonary metastases in MPA-treated mice but only 13% of metastases in untreated mice. Mice receiving at least 1-mg doses of MPA gained more weight than control-treated mice but exhibited no bone density alterations or abnormal mammary fat pad histology. Conclusion: Our preclinical results show that MPA appears to elevate Nm23-H1 metastasis suppressor gene expression, thereby reducing metastatic colonization. The data suggest a new use for an old agent in a molecularly defined subset of breast cancer patients.

Sign in / Sign up

Export Citation Format

Share Document