Barrett’s esophagus (BE) is a precancerous lesion of esophageal adenocarcinoma (EAC). It is a pathological change in which the squamous epithelium distal esophagus is replaced by columnar epithelium. Loss of P53 is involved in the development of BE and is taken as a risk factor for the progression. We established a HET1A cell line with P53 stably knockdown by adenovirus vector infection, followed by 30 days of successive acidic bile salt treatment. MTT, transwell assay, and wound closure assay were applied to assess cell proliferation and migration ability. The expression of key factors was analyzed by RT-qPCR, western blotting and immunohistochemical staining. Our data show that the protein expression level of P53 reduced after exposure to acidic bile salt treatment, and the P53 deficiency favors the survival of esophageal epithelial cells to accommodate the stimulation of acidic bile salts. Furthermore, exposure to acidic bile salt decreases cell adhesions by repressing the JAK/STAT signaling pathway and activating VEGFR/AKT in P53-deficient esophageal cells. In EAC clinical samples, P53 protein expression is positively correlated with that of ICAM1 and STAT3 and negatively correlated with VEGFR protein expression levels. These findings elucidate the role of P53 in the formation of BE, explain the mechanism of P53 deficiency as a higher risk of progression for BE formation, and provide potential therapeutic targets for EAC.

Background: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a common inflammatory disorder with high postoperative recurrence rates. The nasopharyngeal microbiome may play a role in disease pathogenesis, but its diagnostic and prognostic utility remains unclear. This study characterized the nasopharyngeal microbiota in CRSwNP patients and evaluated its potential as a biomarker. Methods: 32 nasopharyngeal swab samples from CRSwNP patients and 11 from controls were collected and subjected to 16S rRNA gene sequencing. Microbial diversity, species composition, and differential abundance were analyzed. A diagnostic model was constructed using LASSO regression, with feature selection performed entirely within a 10-fold cross-validation framework, and model stability was validated via 100 Bootstrap resampling iterations. For recurrence prediction, due to the limited number of events (n=10), only exploratory univariate screening was conducted, and the stability of candidate biomarkers was evaluated using Bootstrap validation with internal feature selection (300 iterations). Results: CRSwNP patients exhibited significantly altered microbial composition at phylum and genus levels, as well as higher Shannon and Chao1 indices compared with controls, although the clinical and biological significance of this diversity increase requires further investigation. The three-genus combined diagnostic panel consisting of Fibrobacter , Ruminococcaceae_UCG-002 , and Staphylococcus demonstrated favorable diagnostic performance. For recurrence prediction, Helicobacter and Parabacteroides were identified as stable candidate biomarkers, with Bootstrap selection frequencies of 24.0% and 27.3%, respectively. The recurrence-related findings are exploratory hypothesis-generating results and do not possess clinical predictive capability; they require validation in an independent large-cohort study. Conclusions: The nasopharyngeal microbiota of CRSwNP patients exhibited significant alterations. The three-genus combined diagnostic panel demonstrated good discriminatory ability, supporting its potential as a non-invasive diagnostic biomarker. The identification of recurrence-related markers provides candidate targets for future research; however, due to the limited sample size, they currently lack clinical predictive capability. This study provides foundational data for microbiome research and clinical translation in CRSwNP.