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DDX46, a member of DEAD‐box (DDX) proteins, is associated with various cancers, while its involvement in the pathogenesis of breast cancer hasn't been reported so far. The study demonstrated the overexpression of DDX46 in human breast cancer cells and tissue samples, and correlated with high histological grade and lymph node metastasis. Downregulation of DDX46 in the breast cancer cell lines inhibited their proliferation and invasiveness in vitro. Furthermore, the growth of MDA‐MB‐231 xenografts was suppressed in nude mice by DDX46 knockingdown. Taken together, our findings suggest that DDX46 is an oncogenic factor in human breast cancer, and a potential therapeutic target. [ABSTRACT FROM AUTHOR]

A new 2 D Cu(II)-based coordination polymer (CP) {[Cu5(Hcia)4(dpp)2(H2O)2(μ-OH)2]·2H2O}n (1) was designed and synthesized via using the mixed-ligand strategy, using 1,3-di(4-pyridyl)propane (dpp) colinker with a flexible spacer H3cia (H3cia: 5-(2-carboxybenzyloxy)isophthalic acid). Furthermore, we use the grinding method to downsize the complex 1 to nano-region (denoted as nano 1 hereafter). Furthermore, in order to determine the inhibitory effect of nano 1 on the viability of the BT474 breast cancer cells, the Cell Counting Kit-8 (CCK-8) was performed firstly. Then, the Annexin V-FITC/PI staining method was used to evaluate the BT474 breast cancer cells apoptosis levels after treated with nano 1. Next, the reactive oxygen species (ROS) detection kit was used in this study to determine the ROS level in the cancer cells after nano 1 treatment. By calculating posture scores and docking, the latent binding pattern of compound to receptor DNA were explored. [ABSTRACT FROM AUTHOR]

Myc proto-oncogene (MYC) is an oncoprotein that promotes proliferation and apoptosis. MYC mutations frequently disrupt the apoptotic processes during tumorigenesis. In the present study, the effects of the MYC point mutation T58A on the progression of a cellular tumor antigen p53 (p53)−/− human breast cancer cell line was analyzed, and the mechanism of p53-independent MYC-induced apoptosis was investigated. HCC1937 cells were transfected with mutant (T58A) or wild-type (WT) MYC using lentiviral vectors. The proliferation of transfected cells was evaluated by colony formation and MTT assays, and apoptosis was analyzed by flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assays. WT MYC was transfected into HCC1937 cells exhibiting p14/p21 silencing through lentivirus-mediated RNA interference. The expression levels of Bim were detected by reverse transcription-quantitative polymerase chain reaction and western blot analyses. Mutant MYC proteins retained the ability to stimulate the proliferation of HCC1937 cells, although they were defective at promoting apoptosis due to a failure to induce the Bcl-2 homology 3 domain-only protein Bim. When p14 was silenced, the effects of mutant MYC on proliferation and apoptosis were weakened. When p21 was silenced, the effects of mutant MYC were strengthened. Breast cancer-derived T58A MYC mutations are unable to activate Bim due to their failure to regulate p14/p21. It was concluded that mutant MYC was more effective compared with WT MYC at promoting the progression of breast cancer. [ABSTRACT FROM AUTHOR]

5A on p. 6271, the "hUMSCs" and "hUMSCs/vector" panels appeared to show overlapping sections of data, such that they were likely to have been derived from the same original source where the results of differently performed experiments were intended to have been shown. 5, now including the correct data panel for the "hUMSCs/vector" experiment, is shown opposite. Oncol Lett 15: 6265-6274, 2018; DOI: 10.3892/ol.2018.8166 Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that, for the histology experiments shown in Fig. [Extracted from the article]

(A) Inhibition of migration and invasion of cancer cells in coculture with hUMSCs/IL-18, hUMSCs/vector or hUMSCs (stained with crystal violet). (B) Compared with hUMSCs/vector and hUMSCs, hUMSCs/IL-18 markedly suppressed the migration and invasion of the MCF-7 cells (* P<0.001). Exp Ther Med 9:1192-1200, 2015; DOI: 10.3892/etm.2015.2286 Subsequently to the publication of the above article, a concerned reader drew to the authors' attention that, with the invasion and migration assay data shown in Fig. [Extracted from the article]

Development of an improved breast cancer therapy has been an elusive goal of cancer gene therapy for a long period of time. Human mesenchymal stem cells derived from umbilical cord (hUMSCs) genetically modified with the interleukin (IL)-18 gene (hUMSCs/IL-18) were previously demonstrated to be able to suppress the proliferation, migration and invasion of breast cancer cells in vitro. In the present study, the effect of hUMSCs/IL-18 on breast cancer in a mouse model was investigated. A total of 128 mice were divided into 2 studies (the early-effect study and the late-effect study), with 4 groups in each, including the PBS-, hUMSC-, hUMSC/vector- and hUMSC/IL-18-treated groups. All treatments were injected along with 200 µl PBS. Following therapy, the tumor size, histological examination, and expression of lymphocytes, Ki-67, cluster of differentiation 31 and cytokines [interleukin (IL)-18, IL-12, interferon (IFN)-γ and TNF-α] in each group were analyzed. Proliferation of cells (assessed by measuring tumor size and Ki-67 expression) and metastasis, (by determining pulmonary and hepatic metastasis) of breast cancer cells in the hUMSC/IL-18 group were significantly decreased compared with all other groups. hUMSCs/IL-18 suppressed tumor cell proliferation by activating immunocytes and immune cytokines, decreasing the proliferation index of proliferation marker protein Ki-67 of tumor cells and inhibiting tumor angiogenesis. Furthermore, hUMSCs/IL-18 were able to induce a more marked and improved therapeutic effect in the tumor sites, particularly in early tumors. The results of the present study indicate that hUMSCs/IL-18 were able to inhibit the proliferation and metastasis of breast cancer cells in vivo, possibly leading to an approach for a novel antitumor therapy in breast cancer. [ABSTRACT FROM AUTHOR]

Highlights: [•] Spontaneous breast cancer TA2 mouse was used as model of TNBC. [•] Tumor immunotherapy manifested strong killing activity against TNBC. [•] The effect of GM-CSF combined with antigens and CpG was better than DC–CIK cells. [ABSTRACT FROM AUTHOR]