LABORATORY RESEARCH DOT1L Cooperates with the c-Myc-p300 Complex to Epigenetically Derepress CDH1 Transcription Factors in Breast Cancer Progression Scientists identified that DOT1L cooperates with c-Myc and p300 acetyltransferase to epigenetically activate epithelial–mesenchymal transition regulators in breast cancer progression. [Nat Commun] Full Article Disrupting Na+,HCO3−-Cotransporter NBCn1 (Slc4a7) Delays Murine Breast Cancer Development Genome-wide association studies have indicated a possible link between the Na+,HCO3−-cotransporter NBCn1 and breast cancer. Researchers tested the functional consequences of NBCn1 knockout for breast cancer development. [Oncogene] Abstract Deacetylation of HSPA5 by HDAC6 Leads to GP78-Mediated HSPA5 Ubiquitination at K447 and Suppresses Metastasis of Breast Cancer Researchers identified that the specific lysine residue 447 (K447) of heat-shock protein 5 (HSPA5) could be modified with polyubiquitin for subsequent degradation through the ubiquitin proteasomal system, leading to the suppression of cell migration and invasion of breast cancer. [Oncogene] Abstract PKCζ Promotes Breast Cancer Invasion by Regulating Expression of E-Cadherin and Zonula Occludens-1 (ZO-1) via NFκB-p65 Investigators report a possible mechanism of oncogenic protein kinase C zeta (PKCζ) signaling in the context of breast cancer. They observed that depletion of PKCζ promotes epithelial morphology in mesenchymal-like MDA-MB-231 cells. [Sci Rep] Full Article Anti-Angiogenesis Therapy and Gap Junction Inhibition Reduce MDA-MB-231 Breast Cancer Cell Invasion and Metastasis In Vitro and In Vivo Scientists evaluated avastin, an anti-VEGF antibody; and oleamide, a gap junction inhibitor, using MDA-MB-231 human breast cancer cells in vitro and a xenograft murine model in vivo. [Sci Rep] Full Article Identification of Estrogen Response Element in Aquaporin-3 Gene that Mediates Estrogen-Induced Cell Migration and Invasion in Estrogen Receptor-Positive Breast Cancer The authors investigated whether aquaporin-3 (AQP3), one of the aquaporins expressed highly in breast cancer, had any clinical implication in estrogen-receptor positive breast cancer, and explored the regulatory mechanisms of AQP3 in estrogen-related breast cancer progression. [Sci Rep] Full Article Epiregulin Contributes to Breast Tumorigenesis through Regulating Matrix Metalloproteinase 1 and Promoting Cell Survival Gene knock-down approaches using shRNA-based strategies were used to determine the requirement of epidermal growth factor family member epiregulin (EREG) for growth of MCF10DCIS cells in vivo, and for identifying mechanisms through which EREG promotes tumor cell survival. [Mol Cancer] Full Article Interactions between αv-Integrin and HER2 and Their Role in the Invasive Phenotype of Breast Cancer Cells In Vitro and in Rat Brain Clones of MDA-MB231BR human breast cancer cells with stable knock down of αv-integrin in combination with high or low levels of HER2 were created. The interactions of these two proteins and their combined effect on cell migration and invasion were investigated in vitro and in vivo. [PLoS One] Full Article CLINICAL RESEARCH Aromatase Inhibitors versus Tamoxifen in Early Breast Cancer: Patient-Level Meta-Analysis of the Randomized Trials The authors undertook meta-analyses of individual data on 31,920 postmenopausal women with estrogen-receptor-positive early breast cancer in the randomized trials of five years of aromatase inhibitor versus five years of tamoxifen; of five years of aromatase inhibitor versus two to three years of tamoxifen then aromatase inhibitor to year five; and of two to three years of tamoxifen then aromatase inhibitor to year five versus five years of tamoxifen. [Lancet] Full Article Long-Term Safety and Anti-Tumor Activity of Olaparib Monotherapy after Combination with Carboplatin and Paclitaxel in Patients with Advanced Breast, Ovarian or Fallopian Tube Cancer Patients had first participated in a Phase I study of olaparib combined with carboplatin and/or paclitaxel. They continued with olaparib monotherapy in their best interest if they failed to tolerate the combination due to the treatment-related adverse events. [Br J Cancer] Abstract |