Leonard Lothstein^*, Judith Soberman^†, Deanna Parke^*, Jatin Gandhi^*, Trevor Sweatman^‡, Tiffany Seagroves^*

Oncology Research, Vol.28, No.5, pp. 451-465, 2020, DOI:10.3727/096504020X15898794315356

Abstract Triple-negative breast cancer (TNBC) is unresponsive to antiestrogen and anti-HER2 therapies, requiring the use of cytotoxic drug combinations of anthracyclines, taxanes, cyclophosphamide, and platinum compounds. Multidrug therapies achieve pathological cure rates of only 20–40%, a consequence of drug resistance and cumulative dose limitations necessitated by the reversible cardiotoxic effects of drug therapy. Safer and more effective treatments for TNBC are required to achieve durable therapeutic responses. This study describes the mechanistic analyses of the novel anthracycline, pivarubicin, and its in vivo efficacy against human primary TNBC. Pivarubicin directly activates PKCd, triggers rapid mitochondrial-dependent apoptosis, and… More >

Guoqiang Zhang^*1, Zengyan Liu^†1, Yong Han^*, Xiaohong Wang^*, Zhenlin Yang^*

Oncology Research, Vol.24, No.4, pp. 233-238, 2016, DOI:10.3727/096504016X14648701447977

Abstract Triple-negative breast cancer (TNBC) is associated with high recurrence rates of metastasis and death. miR-509 has been reported to be a tumor suppressor in many cancers, but its effect in TNBC has not yet been identified. In this article, we explored the effects of miR-509 on the malignant phenotype of TNBC cells, including proliferation, apoptosis, migration, and invasion. We transiently transfected TNBC cells, Hs578T, with miR-509 mimic. Upon transfection, the expression of miR-509 was upregulated about 50-fold compared with cells transfected with scramble mimic. Overexpression of miR-509 inhibited cell proliferation, induced cell apoptosis, and suppressed More >