This study aimed to describe the use of a novel 4-lncRNA signature to predict prognosis in patients with laryngeal cancer and to explore its possible mechanisms. We identified lncRNAs that were differentially expressed between 111 tumor tissue samples and 12 matched normal tissue samples from The Cancer Genome Atlas Database (TCGA). We used Cox regression analysis to identify lncRNAs that were correlated with prognosis. A 4-lncRNA signature was developed to predict the prognosis of patients with laryngeal cancer. The receiver operating characteristic (ROC) curves and area under the curve (AUC) were used to verify the validity of this Cox regression model, and an independent prognosis analysis was used to confirm that the 4-lncRNA signature was an independent prognostic factor. Furthermore, the function of these lncRNAs was inferred using related gene prediction and Gene ontology (GO) enrichment analysis in order to clarify the possible mechanisms underlying their predictive ability. In total, 214 differentially expressed lncRNAs were identified, and a 4-lncRNA signature was constructed using Cox survival analysis. The risk coefficients in the multivariate Cox analysis revealed that LINC02154 and MNX1-AS1 are risk factors for laryngeal cancer, whereas MYHAS and LINC01281 appear to be protective factors. The results of a functional annotation analysis suggested that the mechanisms by which these lncRNAs influence prognosis in laryngeal cancer may involve the extracellular exosome, the Notch signaling pathway, voltage-gated calcium channels, and the Wnt signaling pathway. We identified a novel 4-lncRNA signature that can predict the prognosis of patients with laryngeal cancer and that may influence the prognosis of laryngeal cancer by regulating immunity, tumor apoptosis, metastasis, invasion, and other characteristics through the Notch signaling pathway, voltage-gated calcium channels, and the Wnt signaling pathway.

Background: Previous observational studies have reported inconsistent findings regarding the incidence of cancer in patients with schizophrenia compared to the general population. The causal relationship between schizophrenia and cancer remains unclear and requires further investigation.Objective: To investigate the causal relationship between schizophrenia and cancer.Methods: In this study, a two-sample Mendelian randomization (MR) analysis was conducted using publicly available genome-wide association studies to determine the causal relationship. The effect estimates were calculated using the random-effects inverse-variance-weighted method.Results: We determined a causal relationship between genetic predisposition to schizophrenia and cancer, with schizophrenia increasing lung cancer (odds ratio (OR) = 1.0007; 95% confidence interval (CI), 1.0001-1.0013; p = 0.0192), thyroid cancer (OR = 1.5482; CI, 1.1112-2.1569; p =0.0098),colorectal cancer (OR = 1.0009; CI, 1.0001-1.0018; p = 0.0344), ovarian cancer (OR = 1.0770; CI, 1.0352-1.1203; p = 0.0002), breast cancer (OR = 1.0011; CI, 1.0001- 1.0022; p =0.0352) and reduced the risk of malignant neoplasm of the stomach (OR = 0.8502; CI, 0.7230-0.9998; p = 0.0496).Conclusions: This study conducted a two-sample MR analysis and discovered a positive causal relationship between schizophrenia and breast, ovarian, thyroid, lung, and colorectal cancers. On the other hand, an inverse causal relationship was found between schizophrenia and malignant neoplasm of the stomach.

Purpose This study aimed to investigate the effects of activating transcription factor-5 (ATF5) on nasopharyngeal carcinoma (NPC) cell radioresistance. Methods HONE-1 nasopharyngeal carcinoma cells were irradiated by conventional fractionation to generate HONE-1R radiotherapy-resistant cells. Short hairpin RNA (shRNA) expression plasmids targeting the ATF5 gene were constructed and transfected into the HONE-1R cell line. The proliferation assay, colony formation analysis, Transwell Boyden chamber assay and other experimental methods were performed to verify changes in the radiosensitivity and other biological of NPC cells. Results X-ray irradiation significantly promoted the upregulation of ATF5 protein levels in HONE-1 cells, and the protein expression of ATF5 increased with the dose of X-ray irradiation (p < 0.05). The colony formation rate, cell survival rate and migration ability of HONE-1R cells were significantly higher than those of HONE-1 cells (p < 0.05). Simultaneously, X-ray could also promote the morphology of epithelial-mesenchymal transition (EMT) in HONE-1 cells, inducing a lower expression level of E-cadherin and a higher expression level of N-cadherin in a dose-dependent manner (p < 0.05). Inhibiting ATF5 significantly reduced the colony formation rate, cell survival rate, migration and invasiveness of HONE-1R cells (p < 0.05). Moreover, sensitizing HONE-1R cells to X-ray irradiation significantly upregulated the expression of E-cadherin and downregulated the expression of N-cadherin in these cells (p < 0.05). Conclusions ATF5 may be a potential therapeutic target to improve radiosensitivity in NPC.

While numerous studies have investigated the association between alkaline phosphatase (ALP) levels and the prevalence of cancer, the epidemiological evidence regarding the relationship between ALP and specific cancer types, as well as cancer prognosis, remains inconclusive. This study aimed to fill this gap. This study employed retrospective cohort design utilizing data from the National Health and Nutrition Examination Survey (NHANES) database, covering the period from 2003 to 2016. Mortality data up to December 31, 2017, were retrieved from the National Death Index (NDI). Weighted multivariable logistic regression and restricted cubic spline (RCS) plots were employed to explore nonlinear associations between ALP levels and cancer. Additionally, weighted Cox proportional hazards models and Kaplan-Meier (KM) curves were used to analyze the relationship between ALP levels and all-cause mortality, as well as specific-cause mortality. Subgroup analyses were conducted to assess the consistency of the results. The study included 21,698 participants, with an average age of 47.21 ± 0.27 years, of whom 51.39% were female and 2064 had cancer. Participants were categorized into three models (crude model to model 2) based on different adjustment variables. Fully adjusted weighted logistic regression analysis revealed positive association between ALP levels and higher cancer prevalence (OR: 1.15, 95% CI: 1.00-1.19, P = 0.002). Consistent trend was observed across ALP quartiles (Q4 vs. Q1 OR: 1.42, 95% CI: 1.19–1.70, P for trend < 0.001). The smooth curve fitting model confirmed linear increasing trend between cancer prevalence and ALP levels (P for nonlinearity = 0.390). Further analysis by cancer type indicated that ALP levels were associated with breast cancer (OR: 1.09, 95% CI: 1.05–1.14), digestive system cancers (OR: 1.06, 95% CI: 1.01–1.11), urinary system cancers (OR: 1.05, 95% CI: 1.02–1.08), bone tumors (OR: 1.01, 95% CI: 1.01–1.02), and other cancer types (OR: 1.08, 95% CI: 1.05–1.10). Additionally, the results of multivariable Cox regression analysis showed that the hazard ratio (HR) for all-cause mortality in the Q4 group was 1.81 (95% CI: 1.55–2.12), and the HR for cancer-specific mortality was 1.40 (95% CI: 1.02–1.91). However, no significant trend was observed for cardiovascular mortality (P > 0.05). The KM survival curves for all-cause mortality, cancer-specific mortality, and heart-cause mortality indicated that the mortality rate for individuals in Group Q4 was significantly higher (P log-rank < 0.05). Stratified analysis results showed no significant interaction effects for variables, except for age and LDH (P for interaction > 0.05). Our study indicates that elevated ALP levels are associated with higher prevalence of cancer. Additionally, ALP levels possess significant clinical value in predicting the risks of all-cause and cancer-specific mortality among American adults. Further prospective studies are needed to confirm these results.

Sleep disorders significantly impact the quality of life for many individuals, which remain largely unrecognized. It is widely believed that dietary nutrient intake plays a crucial role in promoting healthy sleep patterns. However, there is lack of research focusing on cancer survivors. This study utilized the National Health and Nutrition Examination Survey (NHANES) database to investigate the correlation between dietary nutrient intake and sleep disorders in cancer survivors. Analyzing data from 2882 cancer survivors in NHANES spanning from 2005 to 2018. Dietary nutrient intake was evaluated through two 24-h dietary recalls. Weighted multivariable logistic regression model was employed to further applied to explore the association between dietary fiber intake and sleep disorders while controlling for relevant confounding factors. Additionally, the nonlinear and dose–response relationships were explored using restricted cubic spline (RCS) regression along with smooth curve fitting and threshold effect analysis. Stratified analysis and interaction analysis were conducted to assess the consistency of the results. Univariable and multivariable analysis demonstrated that dietary fiber intake showed negative correlation with sleep disorders (P < 0.05). Treating dietary fiber intake as continuous variable. After accounting for all covariates, the study reaffirmed the protective role of dietary fiber (odds ratio [OR]: 0.99, 95% confidence interval [CI]: 0.98–0.99, P = 0.044). Analysis of dietary fiber intake in quartiles further supported this trend (P < 0.001). Interestingly, further investigations indicated that dietary fiber intake was not associated with sleep apnea, insomnia, restless legs syndrome, or other types of sleep disorders (P > 0.05). Notably, no statistically significant interactions were observed in all subgroup analyses except poverty income ratio (PIR) (P for interaction < 0.05), indicating that the protective effect of dietary fiber on sleep disorders was more pronounced in individuals with PIR ≥ 2.5. Our results suggest that adequate dietary fiber intake may be beneficial dietary strategy to reduce sleep disorders in cancer survivors.