Despite the tremendous efforts of many researchers and clinicians, cancer remains the second leading cause of mortality worldwide. Mesenchymal stem/stromal cells (MSCs) are multipotent cells residing in numerous human tissues and presenting unique biological properties, such as low immunogenicity, powerful immunomodulatory and immunosuppressive capabilities, and, in particular, homing abilities. Therapeutic functions of MSCs are mediated mostly by the paracrine effect of released functional molecules and other variable components, and among them the MSC-derived extracellular vesicles (MSC-EVs) seem to be one of the central mediators of the therapeutic functions of MSCs. MSC-EVs are membrane structures secreted by the MSCs, rich in specific proteins, lipids, and nucleic acids. Amongst these, microRNAs have achieved the most attention currently. Unmodified MSC-EVs can promote or inhibit tumor growth, while modified MSC-EVs are involved in the suppression of cancer progression via the delivery of therapeutic molecules, including miRNAs, specific siRNAs, or suicide RNAs, as well as chemotherapeutic drugs. Here, we present an overview of the characteristics of the MSCs-EVs and describe the current methods for their isolation and analysis, the content of their cargo, and modalities for the modification of MSC-EVs in order for them to be used as drug delivery vehicles. Finally, we describe different roles of MSC-EVs in the tumor microenvironment and summarize current advances of MCS-EVs in cancer research and therapy. MSC-EVs are expected to be a novel and promising cell-free therapeutic drug delivery vehicle for the treatment of cancer.

Breast cancer (BC) remains one of the most prevalent and life-threatening malignancies worldwide, marked by significant heterogeneity and complex mechanisms of progression. Despite major advances in understanding its molecular and cellular basis, the processes driving tumor progression and metastasis continue to challenge effective treatment. Among the emerging research areas, extracellular vesicles (EVs) have gained considerable attention for their key role in intercellular communication and their contribution to cancer biology. In BC, tumor cell-derived EVs are implicated in multiple processes that promote disease progression, including tumor growth, remodeling of the tumor microenvironment, and facilitation of metastasis. By transferring oncogenic signals to recipient cells, EVs critically shape the metastatic niche and support the spread of cancer cells to distant organs. Recent studies highlight the diverse functions of BC-derived EVs in modulating immune responses, inducing angiogenesis, and enhancing cancer cell invasiveness. This review explores the role of BC-derived EVs in tumor progression and metastasis. We discuss their molecular composition, mechanisms of action, and impact on the tumor microenvironment, aiming to provide insights into their role in BC pathophysiology and discuss potential clinical applications. A deeper understanding of the complex interplay between EVs and cancer progression may pave the way for innovative strategies to combat BC and improve patient outcomes.

The human uterine tube serves not only as an organ for gamete transportation and fertilization but also provides a suitable microenvironment for early embryonic development. Mentioned events could not function without the activity of uterine tube epithelial cells (UTECs) and stromal cells, which respond to ovarian estrogen and progesterone. In our experiment, we modeled steroid hormone concentration dynamics as they progress towards the so-called window of implantation (WOI) using human UTEC monolayer cultures and hormonal cell treatment (estrogen and progesterone). Subsequently, human UTECs underwent Quantitative Real-Time PCR (qPCR), and their secretome content was also analyzed using multiplex immunoaffinity analysis on the Luminex MAGPIX ^® platform. Our results highlight the immunomodulatory, angiogenic, and tissue-remodeling factors of UTEC in response to dynamic hormonal changes, as observed from the peri-ovulatory phase through the WOI. The main time points have been the hormonal switch at the beginning of Day 3 and the end of Day 7. The physiological hormonal transition induced a distinct temporal response, marked by early activation of remodeling and angiogenic pathways (BMP4, SPP1, VEGFA, TGIF2) followed by their stabilization, while immune-related genes displayed progressive activation, particularly between Days 3 and 7. Notably, the experimental cultures exhibited the strongest induction of CXCL8, IL-1B, and IL-16 compared with both control conditions, indicating the establishment of a controlled immunomodulatory environment. Similarly, MAGPIX results corroborated the findings, with elevated IL-11 and TNF-B on Day 7. This phenomenon corresponds to the “inflammatory paradox” that typically occurs during embryo implantation, accompanied by the production of angiogenic and tissue remodeling factors such as VEGFA, BMP4, SPP1, TGIF2, and MMPs. These results demonstrate, in a human in vitro cell model, the clinical importance of a stable uterine tube microenvironment for the onset and maintenance of the early stages of physiological gestation, and provide unique insights into the molecular peculiarities of the uterine tube during this period.