Elevated expression of the inducible heat shock protein 70 (Hsp70) is known to correlate with poor prognosis in many cancers. Hsp70 confers survival advantage as well as resistance to chemotherapeutic agents, and promotes tumor cell invasion. At the same time, tumor-derived extracellular Hsp70 has been recognized as a “chaperokine”, activating antitumor immunity. In this review we discuss localization dependent functions of Hsp70 in the context of invasive cancer. Understanding the molecular principles of metastasis formation steps, as well as interactions of the tumor cells with the microenvironment and the immune system is essential for fighting metastatic cancer. Although Hsp70 has been implicated in different steps of the metastatic process, the exact mechanisms of its action remain to be explored. Known and potential functions of Hsp70 in controlling or modulating of invasion and metastasis are discussed.

Particulate matter (PM), a complex mixture of solid particles and liquid droplets, originates from both natural sources, such as sand, pollen, and marine salts, and anthropogenic activities, including vehicle emissions and industrial processes. While PM itself is not inherently toxic in all its forms, it often acts as a carrier of xenobiotic toxicants, such as heavy metals and organic pollutants, which adhere to its surface. This combination can result in synergistic toxic effects, significantly enhancing the potential harm to biological systems. Due to its small size and composition, PM can penetrate deep into the respiratory tract, acting as a physical “shuttle” that facilitates the distribution and bioavailability of toxic substances to distant organs. The omnipresence of PM in the environment leads to unavoidable and constant exposure, contributing to increased morbidity and mortality rates, particularly among vulnerable populations like the elderly, children, and individuals with pre-existing health conditions. This exposure also imposes a substantial financial burden on healthcare systems, as treating PM-related illnesses requires significant medical resources and leads to higher healthcare costs. Addressing these challenges necessitates effective mitigation strategies, including reducing PM exposure, improving air quality, and exploring novel approaches such as AI-based exposure prediction and nutritional interventions to protect public health and minimize the adverse effects of PM pollution.

The glycosylphosphatidylinositol (GPI)-anchored molecule CD59 has been implicated in the modulation of T cell responses, but the underlying molecular mechanism of CD59 influencing T cell signaling remained unclear. Here we analyzed Jurkat T cells stimulated via anti-CD3ε- or anti-CD59-coated surfaces, using time-resolved single-cell Ca²⁺ imaging as a read-out for stimulation. This analysis revealed a heterogeneous Ca²⁺ response of the cell population in a stimulus-dependent manner. Further analysis of T cell receptor (TCR)/CD3 deficient or overexpressing cells showed that CD59-mediated signaling is strongly dependent on TCR/CD3 surface expression. In protein co-patterning and fluorescence recovery after photobleaching experiments no direct physical interaction was observed between CD59 and CD3 at the plasma membrane upon anti-CD59 stimulation. However, siRNA-mediated protein knock-downs of downstream signaling molecules revealed that the Src family kinase Lck and the adaptor molecule linker of activated T cells (LAT) are essential for both signaling pathways. Furthermore, flow cytometry measurements showed that knock-down of Lck accelerates CD3 re-expression at the cell surface after anti-CD59 stimulation similar to what has been observed upon direct TCR/CD3 stimulation. Finally, physically linking Lck to CD3ζ completely abolished CD59-triggered Ca²⁺ signaling, while signaling was still functional upon direct TCR/CD3 stimulation. Altogether, we demonstrate that Lck mediates signal transmission from CD59 to the TCR/CD3 pathway in Jurkat T cells, and propose that CD59 may act via Lck to modulate T cell responses.

A poly(dimethylsiloxane) (PDMS)-based biochip with an integrated pressure controlled positioning system with sub-micrometre precision was realized. The biochip was easy and cheap to manufacture and enabled positioning in a wet environment. It allowed the application of total internal reflection fluorescence (TIRF) microscopy at the dorsal cell membrane, which is not adhering to a support. Specifically, the chip enabled TIRF microscopy at the apical membrane of polarized epithelial cells. Thereby, the device allowed us for the first time to monitor individual fusion events of GPI–GFP bearing vesicles at the apical membrane in live Madin–Darby canine kidney II (MDCK II) cells. Moreover, a mapping of fusion sites became feasible and revealed that the whole apical membrane is fusion competent. In total, the biochip offers an all-in-one solution for apical TIRF microscopy and contributes a novel tool to study trafficking processes close to the apical plasma membrane in polarized epithelial cells.

Plastics are highly persistent materials, and their environmental degradation can potentially exacerbate, rather than alleviate, pollution. The degradation of plastic materials releases toxic monomers and additives, such as bisphenol A (BPA), styrene, and dioxins, which are more reactive, harmful, and persistent than intact plastics. With half-lives ranging from weeks to decades, they bioaccumulate in food chains, disrupt ecosystems, and contribute to endocrine disruption and mutagenicity. Natural degradation pathways, like microbial metabolism and photodegradation, are slow and incomplete, often leaving toxic intermediates such as microplastics. Artificial strategies, including bioremediation and advanced oxidation processes (AOPs), show potential to address the problems of plastic pollution but face additional challenges like secondary pollution and scalability. Sustainable alternatives, including bioplastics and renewable non-plastic substitutes, present promising solutions. However, their widespread adoption is hindered by challenges such as high production costs and the need for specific conditions to facilitate degradation, necessitating further research and development. A combined approach of reducing plastic production, advancing recycling, and implementing effective remediation strategies is critical to mitigating plastic pollution’s long-term impacts on ecosystems, biodiversity, and human health. This review provides a critical analysis of the current understanding of plastic degradation processes and the toxic byproducts they generate. It highlights the paradox wherein increased degradability may exacerbate environmental hazards. Additionally, the review assesses innovative, eco-friendly alternatives designed to mitigate plastic pollution.