Focal adhesion plaques (FAPs) play an important role in the communication between cells and the extracellular matrix (ECM) and in cells’ migration. FAPs are macromolecular complexes made by different proteins which also interact with matrix metalloproteinases (MMPs). Because of these fundamental properties, FAPs and MMPs are also involved in cancer cells’ invasion and in the metastatic cascade. The most important proteins involved in FAP formation and activity are (i) integrins, (ii) a complex of intracellular proteins and (iii) cytoskeleton proteins. The latter, together with MMPs, are involved in the formation of filopodia and invadopodia needed for cell movement and ECM degradation. Due to their key role in cancer cell migration and invasion, MMPs and components of FAPs are often upregulated in cancer and are thus potential targets for cancer therapy. Polyphenols, a large group of organic compounds found in plant-based food and beverages, are reported to have many beneficial healthy effects, including anticancer and anti-inflammatory effects. In this review, we discuss the growing evidence which demonstrates that polyphenols can interact with the different components of FAPs and MMPs, inhibit various pathways like PI3K/Akt, lower focal adhesion kinase (FAK) phosphorylation and decrease cancer cells’ invasiveness, leading to an overall antitumoral effect. Finally, here we highlight that polyphenols could hold potential as adjunctive therapies to conventional cancer treatments due to their ability to target key mechanisms involved in cancer progression.

Endocrine-disrupting chemicals (EDCs) are chemical substances that can interfere with any hormone action. They are categorized according to origin and use, such as industrial chemicals like polychlorinated biphenyls (PCBs) and polybrominated biphenyls (PBBs), plastics like bisphenol A (BPA), plasticizers like phthalates, pesticides like dichlorodiphenyltrichloroethane (DDT), fungicides like vinclozolin, and pharmaceuticals like diethylstilbestrol (DES). Natural EDCs, such as phytoestrogens, are present in the diet of both humans and animals. Polyphenols are a large group of natural compounds derived from plants and are found in beverages and food. They are grouped based on their chemical structure into flavonoids and nonflavonoids and are reported to have many beneficial effects on health, including, but not limited to, anticancer, antioxidant, and anti-inflammatory effects. Moreover, polyphenols have both pro- and antioxidant characteristics, and due to their antioxidant and anti-inflammatory potential, they presumably have a protective effect against damage induced by EDCs. However, polyphenols may act as EDCs. In this review, we report that polyphenols regulate the activity of EDCs, having both positive and negative effects. Hence, a better understanding of the associations between EDCs and polyphenols will allow the establishment of improved approaches to protect human health from EDCs.

Among the causes of bee colony death, viruses are among the number of pathogens that can contribute to the ill health of a colony. This study focuses on two of the several honeybee viruses, Slow Bee Paralysis Virus-1 (SBPV-1) and Deformed Wing Virus B (DWV-B), both belonging to the Iflavirus genus. To date, there is limited information available on the presence of these viruses in Italy. For this research project (IZS LT 04/19 RC), funded by the Ministry of Health, the presence and positivity of several honeybee viruses were evaluated in Italy using molecular methods. Convenience sampling was used, and these samples were analyzed for the two viruses and/or other main honeybee viruses, using specific PCR protocols and Sanger sequencing when necessary. A statistical analysis was conducted to study the independence between the viruses. Our data demonstrate for the first time the presence of SBPV-1 in Italian territory with a rather low number in most of the regions investigated, except for Emilia-Romagna and Lazio where it was detected more frequently, while DWV-B was detected at a higher level in all the regions investigated.

Cadmium (Cd), a heavy metal known to act as an endocrine disruptor, has been implicated in breast cancer (BC) via mechanisms that involve both estrogen receptor (ER)-dependent and -independent pathways. We used BALB-neuT transgenic mice, a model of aggressive ErbB2-driven mammary carcinogenesis, to evaluate the effects of chronic exposure to an environmentally relevant, low-dose of Cd on tumor onset, multiplicity, progression, immune microenvironment, and metastasis. Cd exposure significantly accelerated tumor onset and increased tumor multiplicity and weight, reducing both tumor-free and overall survival. Cd-exposed mice displayed elevated serum estrogen levels, and increased expression of progesterone receptor and tumor progression markers, including CD31, Ki67, and phosphorylated Akt, in tumor tissues. Despite the increased recruitment of CD4⁺ and CD8⁺ T cells to the peritumoral stroma, Cd exposure fostered an immunosuppressive microenvironment with elevated Tregs and PD-1⁺ exhausted T cells, both locally and systemically. Notably, lung metastases were threefold more frequent in Cd-exposed mice. Our results demonstrate that low-dose Cd exposure promotes the development and progression of ErbB2-driven breast tumors through hormonal, proliferative, and immune-modulating mechanisms. These findings reveal that exposure to environmentally relevant doses of Cd not only accelerates ErbB2-driven breast cancer but also reshapes the immune landscape toward dysfunction and immunosuppression, likely compromising both anti-tumor immunity and response to immunotherapies. These data advocate for tighter regulation of Cd exposure in populations at risk for breast cancer.