Cancer is the second leading cause of death in the world, behind only cardiovascular diseases, and is one of the most serious diseases threatening human health nowadays. Cancer patients’ lives are being extended by the use of contemporary medical technologies, such as surgery, radiotherapy, and chemotherapy. However, these treatments are not always effective in extending cancer patients’ lives. Simultaneously, these approaches are often accompanied with a series of negative consequences, such as the occurrence of adverse effects and an increased risk of relapse. As a result, the development of a novel cancer-eradication strategy is still required. The emergence of nanomedicine as a promising technology brings a new avenue for the circumvention of limitations of conventional cancer therapies. Gold nanoparticles (AuNPs), in particular, have garnered extensive attention due to their many specific advantages, including customizable size and shape, multiple and useful physicochemical properties, and ease of functionalization. Based on these characteristics, many therapeutic and diagnostic applications of AuNPs have been exploited, particularly for malignant tumors, such as drug and nucleic acid delivery, photodynamic therapy, photothermal therapy, and X-ray-based computed tomography imaging. To leverage the potential of AuNPs, these applications demand a comprehensive and in-depth overview. As a result, we discussed current achievements in AuNPs in anticancer applications in a more methodical manner in this review. Also addressed in depth are the present status of clinical trials, as well as the difficulties that may be encountered when translating some basic findings into the clinic, in order to serve as a reference for future studies.

Long noncoding RNA maternally expressed gene 3 (MEG3) involves in fibrotic diseases, but its role in nickel oxide nanoparticles (NiO NPs)-induced pulmonary fibrosis remains unclear. The present study aimed to explore the relationships among MEG3, transforming growth factor-β1 (TGF-β1) and phosphoinositide 3-kinase (PI3K)/AKT pathway in NiO NPs-induced pulmonary fibrosis. Wistar rats were intratracheally instilled with NiO NPs twice a week for 9 weeks, and human lung adenocarcinoma epithelial cells (A549 cells) were exposed to NiO NPs for 24 h. The pathological alterations and increased hydroxyproline indicated that NiO NPs caused pulmonary fibrosis in rats. The up-regulated type I collagen (Col-I) suggested that NiO NPs-induced collagen deposition in A549 cells. Meanwhile, NiO NPs could significantly down-regulate MEG3, up-regulate TGF-β1 and activate PI3K/AKT signaling pathway both in vivo and in vitro. However, we found that the PI3K/AKT pathway activated by NiO NPs could be suppressed by 10 μM TGF-β1 inhibitor (SB431542) in A549 cells. The protein markers (Col-I, Fibronectin, and alpha-smooth muscle actin) of collagen deposition up-regulated by NiO NPs were reduced by 10 μM PI3K inhibitor (LY294002). Furthermore, we further found that overexpressed MEG3 inhibited the expression of TGF-β1, resulting in the inactivation of PI3K/AKT pathway and the reduction of collagen formation. In summary, our results validated that MEG3 could arrest NiO NPs-induced pulmonary fibrosis via inhibiting TGF-β1-mediated PI3K/AKT pathway.

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Type 2 diabetes mellitus (T2DM) is currently a public health problem worldwide and a threat to human health and social development. The incidence rate of the disease is steadily increasing. Various genetic and environmental factors have been established as influencing the pathogenesis of this disease. However, the influence of social factors and the natural environment on DM incidence should also be considered. Low-grade inflammation could represent a central point of connection integrating all these potential triggers, being partly responsible for the development of insulin resistance. This paper aims to elaborate on the impact of the natural environment and social factors on DM development, with a special focus on six aspects of the pathogenesis of DM: pollution, radiation, psychology, drink, sleep, and exercise. We identified a two-way relationship between T2DM and social and natural environments. Changes in these environments may lead to low-grade inflammation, which in turn induces or aggravates T2DM and vice versa. Poor lifestyle may lead to increased insulin resistance and promote DM development. Improvements in blood glucose control can be achieved through nonenvironmental and behavioral interventions.

Supportinginformation and the ORCID identification number(s) for the author(s) of this article can be found under: https://doi.