Lung cancer, one of the most prevalent and deadly malignant tumors, is increasingly common globally in terms of both morbidity and mortality rates. Unlike pyroptosis and necroptosis, cuproptosis is a non-apoptotic programmed cell death process. Studies have demonstrated that cuproptosis is involved in the incidence, development, and metastasis of lung cancer. However, the mechanisms underlying cuproptosis in lung cancer remain to be fully elucidated. In this work, we primarily examine the most recent research on copper homeostasis, cuproptosis mechanisms, and the connection between lung cancer and cuproptosis. A comprehensive literature search was conducted using the Web of Science, PubMed, and Google Scholar databases. The search strategy employed a combination of the keywords "cuproptosis" and "lung cancer." The results encompassed publications from January 2020 to May 2025. This study aimed to gather research focusing on the relationship between lung cancer and cuproptosis, as well as the anticancer effects of drugs that induce cuproptosis. Our research indicates that lung cancer patients experience disruptions in copper ion homeostasis, as well as inhibition of cuproptosis, which points to a potentially effective therapeutic avenue through the induction of cuproptosis in lung cancer cells. This paper provides an overview of the mechanisms that highlight proteins associated with copper homeostasis and genes that play a role in cuproptosis in the lung cancer context. The modulation of proteins such as CTR1, ATOX1, FDX1, CCS, COX17, ATP7A, and ATP7B, in addition to LIPT1 and various long non-coding RNAs (AL691432.2, AC093010.2, AC107464.3, COLCA1, AC026471.3, LINC01833, and ITGB1-DT), along with genes such as DβH, LOXL2, SOD1, UBE2D1, and UBE2D3, can affect these mechanisms. These elements are vital for evaluating clinical interventions for lung cancer patients, predicting risks, and recognizing drug resistance. Moreover, we identified that pharmaceuticals facilitating copper ion transport (elesclomol and disulfiram), copper-chelating agents (DPEN, ATTM, and TETA), and nanoparticles engineered to transport copper are capable of effectively adjusting copper ion concentrations in lung cancer cells, subsequently inducing cuproptosis as a prospective treatment strategy for lung cancer. Furthermore, our findings suggest that lung cancer cells might counteract the harmful impacts of copper buildup by modulating proteins linked to copper metabolism, bolstering the antioxidant defense mechanisms, altering metabolic pathways, and triggering cellular stress responses and repair mechanisms. Cuproptosis represents a novel mechanism dependent on copper that has important implications for the treatment of lung cancer. This process primarily involves the buildup of copper ions, which leads to a disruption in protein homeostasis, ultimately resulting in cell death. Additionally, the abnormal expression of crucial regulatory genes, such as FDX1 and LIPT1, along with transport proteins like CTR1 and ATP7A/B, is closely linked to the advancement of lung cancer. At present, drugs that act as carriers for copper ions (such as elesclomol and disulfiram), metal-organic frameworks based on copper, and copper chelators (including D-penicillamine and ammonium tetrathiomolybdate) have demonstrated promise in eliciting copper-mediated cell death in lung cancer cells. These discoveries suggest new potential targets and strategies for treating lung cancer, which could enhance the prognosis for patients diagnosed with the disease.

Subarachnoid hemorrhage (SAH) is a life‑threatening neurological disease. Recently, inflammatory factors have been confirmed to be responsible for the brain damage associated with SAH. Therefore, studying the post‑SAH inflammatory reaction may clarify the mechanism of SAH. Mitogen and stress‑activated protein kinase 1 (MSK1) causes the phosphorylation of NF‑κB and regulates the activity of pro‑inflammatory transcription factors. The present study aimed to identify the potential role of MSK1 in inflammation and brain damage development following SAH. A cisterna magna blood injection model was established in Sprague‑Dawley rats. Hematoxylin and eosin staining, reverse transcription‑quantitative polymerase chain reaction assays and double immunofluorescence staining were used to analyze the role of MSK1, IL‑1β and TNF‑α in the inflammatory process after SAH. In a model of lipopolysaccharide‑induced astrocyte inflammation, the effect of overexpressing MSK1 overexpression was analyzed by western blot analysis. The results demonstrated that MSK1 expression were negatively correlated with TNF‑α and IL‑1β expression levels, and reached peak levels 2 days after TNF‑α and IL‑1β. The double immunofluorescence staining results showed that the expression of MSK1 was in the same plane of view as TNF‑α and IL‑1β in the brain cortex. Furthermore, the in vitro studies indicated that the overexpression of MSK1 inhibited the expression of TNF‑α and IL‑1β following LPS challenge. These results imply that MSK1 may be involved in the inflammatory reaction following SAH, and may potentially serve as a negative regulator of inflammation.

Accurate nerve identification is critical during surgical procedures for preventing any damages to nerve tissues. Nerve injuries can lead to long-term detrimental effects for patients as well as financial overburdens. In this study, we develop a deep-learning network framework using the U-Net architecture with a Transformer block based fusion module at the bottleneck to identify nerve tissues from a multi-modal optical imaging system. By leveraging and extracting the feature maps of each modality independently and using each modalities information for cross-modal interactions, we aim to provide a solution that would further increase the effectiveness of the imaging systems for enabling the noninvasive intraoperative nerve identification.