Background Breast cancer is the most common type of cancer among women, and despite improved treatments, it remains a major challenge. However, improved mechanistic insight may lead to novel therapeutic strategies. miR‐142‐3p belongs to the miR‐142 family and is involved in pathogenesis and metastasis of various types of malignancies by targeting several important messenger RNAs (mRNAs) including Bach‐1. This is especially true for breast cancer, where Bach‐1 is involved in the metastatic spread by deregulation of metastasis‐associated genes. Methods In this study, we collected 24 breast cancer tissues with 24 adjusted normal tissues to measure the expression levels of miR‐142‐3p and Bach‐1 mRNA using quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR) and IHC. miR‐142‐3p targeting of Bach‐1 expression in MCF‐7 and MDA‐MB‐468 breast cancer cells was evaluated using bioinformatics, qRT‐PCR and western blot analyses. The cellular proliferation, invasion, and migration were assessed by MTT, transwell matrigel and wound healing assay and the EMT‐associated proteins C‐X‐C chemokine receptor type 4 (CXCR‐4), matrix metalloproteinase‐9 (MMP9), and vascular endothelial growth factor receptor (VEGFR) were analyzed by western blot analysis. Also, the expression levels of tumor suppressors including miR‐330, miR‐145, and miR‐34a were estimated by qRT‐PCR. Results Analysis of paired specimens of primary malignant and normal tissues showed that miR‐142‐3p was downregulated, while Bach‐1 mRNA and protein both were overexpressed in the breast cancer tumors. This inverse relationship was confirmed by cell line experiments demonstrating that miR‐142‐3p expression reduced Bach‐1 mRNA levels. Furthermore, replacement of miR‐142‐3p could inhibit the proliferation, invasion, and migration in breast cancer potentially by targeting of Bach‐1 mRNA and subsequent inhibition of CXCR4, MMP9, and VEGFR protein expressions. In addition, induction of miR‐142‐3p could upregulate tumor suppressor miRNAs, including miR‐330, miR‐145, and miR34a. Conclusion For the first time, our results revealed that miR‐142‐3p could target Bach‐1in breast cancer cells leading to the reduction of EMT‐related proteins and reduced cell proliferation, invasion, and migration. The results also demonstrated that miR‐142‐3p could regulate important tumor suppressor miRNAs in breast cancer cells. In conclusion, our results suggest that miR‐142‐3p could be a good candidate for the targeted therapy of breast cancer, especially for the invasive type.

Tumor cells utilize different strategies to communicate with neighboring tissues for facilitating tumor progression and invasion, one of these strategies has been shown to be the release of exosomes. Exosomes are small nanovesicles secreted by all kind of cells in the body, especially cancer cells, and mediate cell to cell communications. Exosomes play an important role in cancer invasiveness by harboring various cargoes that could accelerate angiogenesis. Here first, we will present an overview of exosomes, their biology, and their function in the body. Then, we will focus on exosomes derived from tumor cells as tumor angiogenesis mediators with a particular emphasis on the underlying mechanisms in various cancer origins. Also, exosomes derived from stem cells and tumor‐associated macrophages will be discussed in this regard. Finally, we will discuss the novel therapeutic strategies of exosomes as drug delivery vehicles against angiogenesis.

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This meta-analysis aimed to evaluate the prognostic value of tumor-infiltrating lymphocytes (TILs) and programmed death-ligand 1 (PD-L1), their associations with the clinicopathological characteristics, and the association between their levels in patients with triple-negative breast cancer (TNBC). PubMed, EMBASE, Scopus, ProQuest, Web of Science, and Cochrane Library databases were searched to obtain the relevant papers. Seven studies with 1152 patients were included in this study. Like the level of TILs, there were no significant associations between PD-L1 expression and tumor size, tumor stage, lymph node metastasis, histological grade, and Ki67 (All p-values ≥ 0.05). Furthermore, there was no significant association between PD-L1 expression with overall survival (OS) and disease-free survival (DFS). In assessment of TILs and survival relationship, the results showed that a high level of TILs was associated with long-term OS (hazard ratios (HR) = 0.48, 95% CI: 0.30 to 0.77, p-value < 0.001) and DFS (HR = 0.53, 95% CI: 0.35 to 0.78, p-value < 0.001). The results displayed that tumoral PD-L1 expression was strongly associated with high levels of TILs in TNBC patients (OR = 8.34, 95% CI: 2.68 to 25.95, p-value < 0.001). In conclusion, the study has shown the prognostic value of TILs and a strong association between tumoral PD-L1 overexpression with TILs in TNBC patients.

Fc-fusion proteins are composed of Fc region of IgG antibody (Hinge-CH2-CH3) and a desired linked protein. Fc region of Fc-fusion proteins can bind to neonatal Fc receptor (FcRn) thereby rescuing it from degradation. The first therapeutic Fc-fusion protein was introduced for the treatment of AIDS. The molecular designing is the first stage in production of Fc-fusion proteins. The amino acid residues in the Fc region and linked protein are very important in the bioactivity and affinity of the fusion proteins. Although, therapeutic monoclonal antibodies are the top selling biologics but the application of therapeutic Fc-fusion proteins in clinic is in progress and among these medications Etanercept is the most effective in therapy. At present, eleven Fc-fusion proteins have been approved by FDA. There are novel Fc-fusion proteins which are in pre-clinical and clinical development. In this article, we review the molecular and biological characteristics of Fc-fusion proteins and then further discuss the features of novel therapeutic Fc-fusion proteins.