Esophageal cancer is a lethal disease that frequently occurs in developing countries, the incidence of which could be declined by drinking EGCG-enriched drinks or food. SERPINB2, whose complex functions and regulations are not yet fully understood, are induced by multiple inflammatory molecules and anti-tumor agents. Here, we identify 2444 EGCG-regulated genes in esophageal cancer cells, including SERPINB2. EGCG treatment recruits NF-κB at the promoter and enhancers of SERPINB2 and activates gene transcription, which is repressed by NF-κB knockdown or inhibition. Loss of SERPINB2 leads to a faster migration rate and less expression of Caspase-3 in cancer cells. Our study demonstrates that SERPINB2 is a new tumor-suppressor gene involved in cell movement and apoptosis and could be a therapeutic target for esophageal cancer.

Esophageal cancer (ESCA) is one of the highest lethal malignancy tumors worldwide. Baculoviral IAP repeat-containing protein 3 (BIRC3) is the main inhibitor of apoptosis in many malignancies. The aim of this study was to clarify how BIRC3 acts in ESCA cells. Through TNMplot and GEPIA2 analysis, BIRC3 was found abundantly expressed in ESCA cells. The quantitative RT-PCR assay confirmed BIRC3 was pronouncedly induced in all used ESCA cell lines. In addition, proinflammatory cytokines TNFα and IL-1β were shown to have promotion effects on BIRC3 expression in ESCA cells. These promotive effects were blocked when the function of NF-κB was inhibited by bay 11-7082, which indicates the expression of the BIRC3 gene was regulated via the NF-κB transcription pathway in ESCA. Moreover, bioinformatics analysis showed that the BIRC3 gene had many NF-κB binding cis-elements. Chromatin immunoprecipitation was then performed and it was found that NF-κB directly interacts with cis-elements of the BIRC3 gene. In conclusion, our data proved that the high expression level of BIRC3 maintained the survival of ESCA cells. BIRC3 was up-regulated by proinflammatory cytokine TNFα and IL-1β through the NF-κB signaling pathway, and this may be helpful for esophageal cancer prevention and therapy.

Polyhydroxyalkanoates (PHAs), recognized as a medical biomaterial, have been proven to promote cell proliferation and tissue repair. PHA has a variety of forms: PHB, PHV, PHHx, and PHBHHx, etc. In this study, PHBHHx was selected as the precursor to fabricate biopolyester films. Specifically, a novel type of biopolyester film was generated through an ammonolysis cross-linking reaction in conjunction with polyamidoamine dendrimer G2.0 (PAMAM). The properties of the resultant biopolyester films were comprehensively evaluated, encompassing surface characteristics, amino group content, and water contact angle. The drug-loading properties and compatibility with osteoblasts of the biopolyester films were also determined. The findings revealed that following aminolysis, the biopolyester film surface exhibited enhanced roughness and an enlarged surface area. Moreover, as the aminolysis duration extended, the hydrophilicity and drug-loading efficiency were significantly augmented. Post-aminolysis, the PHBHHx membrane exhibited a more favorable environment for the adhesion and proliferation of osteoblasts. Overall, the biopolyester film developed in this study provides novel insights and materials for tissue engineering, especially bone tissue repair.

The golden apple snail (Pomacea canaliculata) is a globally destructive invasive species. Existing control strategies primarily target adult snails, yet these approaches often fail due to the snails’ robust shells and lack of effective toxicity. To address this problem, extracts from Nerium oleander, Alocasia macrorrhiza, Euphorbia tirucalli and Aconitum carmichaelii were tested on the snail eggs. All four extracts exhibited toxicity at a 75% concentration, with N. oleander being the most potent. Specifically, this extract achieved a 95.42% mortality rate at 75% concentration and induced complete embryonic death at the 50% concentration. All four extracts induced significant oxidative stress-related physiological alterations in the eggs. Notably, N. oleander extract reduced the soluble protein content by 12% and altered key antioxidant enzyme activities (a 1.29-fold increase in SOD and CAT; a 48% decrease in ALT; a 3.52-fold and 5.67-fold increase in AST and POD, respectively). Field trials showed that fresh and dried N. oleander leaf extracts inhibited egg hatching by 96% and 93%, while embryonic observations confirmed developmental impairment. Further, to identify the bioactive components of N. oleander leaf extracts and lay a foundation for subsequent pesticide development, HPLC-MS analysis was performed, and 27 compounds belonging to 7 groups were identified. Collectively, N. oleander treatment induced oxidative stress-related physiological alterations and embryonic developmental impairment, which contributes to its ovicidal outcome. These findings lay a theoretical foundation for plant-derived ovicide development, inform eco-friendly pest management policies, and guide field control practices, highlighting N. oleander as a promising candidate for targeted P. canaliculata egg control.