Lung cancer is the most common malignant tumor with the highest morbidity and mortality in the world, and non-small cell lung cancer (NSCLC) accounts for the vast majority of cases. At present, its main treatment methods are still traditional surgery, radiotherapy and chemotherapy, with disadvantages such as a high recurrence rate and limited effectiveness. Therefore, a new, better treatment method is urgently needed. Gene editing technology, as a new genetic engineering approach, has shown great potential in gene research, gene therapy and genetic improvement. It has also emerged as a promising treatment for lung cancer. This paper reviews the current research and applications of gene editing technology in NSCLC and other aspects of NSCLC, the therapeutic principle and mechanism of action, and the existing problems and prospects. This review aims to provide a basis for the prevention and treatment of NSCLC in the future and improve the survival rate of lung cancer patients.

Objective: The current study aims to elucidate the critical function of hepatocyte nuclear factor 1-beta (HNF1-β) in lupus nephritis (LN) by investigating its modulation of the Derlin-1/valosin-containing protein (VCP)/VCP-interacting membrane selenoprotein (VIMP) complex, endoplasmic reticulum (ER) stress and podocyte apoptosis.Methods: In vitro and in vivo models of LN were established using glomerular podocytes treated with LN serum and MRL/lpr mice, respectively. The expression levels of HNF1-β were analysed in kidney tissues from patients with LN and MRL/lpr mice. To assess the effects of HNF1-β inhibition, an adeno-associated virus vector carrying HNF1-β short hairpin was administered to MRL/lpr mice. In vitro, glomerular podocytes were transfected with HNF1-β small interfering RNA (siRNA) or HNF1-β overexpression plasmids to explore their regulatory effects on the Derlin-1/VCP/VIMP complex and podocyte apoptosis. Dual-luciferase reporter assays and chromatin immunoprecipitation (ChIP) assays were performed to investigate the transcriptional activation of Derlin-1 and VCP promoters by HNF1-β.Results: A significant decrease in HNF1-β levels was observed in kidney tissues from patients with LN while MRL/lpr mice exhibited an initial compensatory increase followed by a subsequent decrease in renal HNF1-β expression. Overexpression of HNF1-β transcriptionally upregulated Derlin-1 and VCP mitigating LN serum-induced ER stress and podocyte apoptosis. In contrast, HNF1-β inhibition exacerbated renal dysfunction and structural damage in MRL/lpr mice. Interestingly, HNF1-β inhibition transcriptionally repressed ERP44, leading to calcium ions (Ca²⁺) release-mediated disruption and inactivation of the Derlin-1/VCP/VIMP complex. This finding suggests that HNF1-β not only regulates the expression of key proteins in the Derlin-1/VCP/VIMP complex but also influences their assembly through Ca²⁺release regulation.Conclusion: This study provides novel insights into the regulatory mechanisms of HNF1-β in LN emphasising its impact on the Derlin-1/VCP/VIMP complex, ER stress and podocyte apoptosis. These findings have the potential to inform the development of new diagnostic tools and therapeutic strategies for LN.

Objective: To investigate the interplay between anxiety disorders and SLE using lupus-prone MRL-lpr mice and MRL/MPJ control mice exposed to predator stress, and to elucidate the potential mechanisms underlying this interaction.Methods: We conducted an experiment where 16 MRL-lpr mice and 16 MRL/MPJ control mice were randomly assigned to four groups and exposed to predator stress (cat exposure) or served as unexposed controls for 2 months. Anxiety levels were evaluated using the elevated plus maze (EPM) and open field test (OFT). Physiological responses were assessed through measurements of body weight, interleukin-6 (IL-6) levels, anti-double-stranded DNA (dsDNA) antibody titres and urine protein content. Additionally, the splenic index and the proportions of regulatory T (Treg) and T helper 17 (Th17) cells were analysed to further understand the immune responses.Results: Both mouse strains exhibited increased anxiety levels as assessed by the EPM and OFT. However, MRL-lpr mice demonstrated a heightened sensitivity to predator stress-induced anxiety compared with MRL/MPJ mice. Biochemical analyses revealed that while MRL/MPJ mice showed a typical inflammatory response to predator stress, characterised by elevated IL-6 levels, this did not exacerbate immune dysregulation or renal damage. In contrast, MRL-lpr mice exhibited markedly increased IL-6 expression, elevated anti-dsDNA antibody levels, higher urine protein content, decreased Treg proportions and increased Th17 proportions in the spleen, suggesting an accelerated progression of lupus disease.Conclusions: Our findings emphasise that lupus-prone MRL-lpr mice display a greater vulnerability to the detrimental consequences of predator stress compared with MRL/MPJ control mice.