scholarly journals SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Emeline Bon ◽  
Virginie Driffort ◽  
Frédéric Gradek ◽  
Carlos Martinez-Caceres ◽  
Monique Anchelin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Suppressor Gene ◽  
Metastasis Suppressor ◽  
Metastasis Suppressor Gene

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 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.

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