RESUMO
In order to determine the underlying mechanism of the senescence occurring in older apple trees, the effects of tree age on the community structure and dominant genus of endophytic rhizosphere bacteria in apple were investigated. The diversity and structure of the bacterial communities and corresponding changes in the dominant genera of endophytic rhizosphere bacteria of apple at different ages (2, 8, 16, 22 years) were compared based on 16S rRNA high-throughput sequencing technology. The results revealed that the longer the tree age, the less the number of ASV in the endophytic bacteria. Moreover, the number of ASV in the endophytic bacteria gradually decreased as the tree age increased, however no significant changes were observed in the alpha diversity. At the phyla level, the relative abundance of Actinobacteria increased, while that of Proteobateria decreased. At the genus level, the relative abundance of Mycobacterium, Chujaibacter, and other genera increased, while the relative abundance of Aquabacterium, Ralstonia, Streptomyces, Asticcacaulis, Hyphomicrobium, Pseudomonas, and Sphingomonas decreased. The reduced relative abundance of endophytic rhizosphere bacteria associated with plant growth and disease resistance may thus be the cause of tree senescence. This work acts as a reference to increases the understanding of plant-microbe interactions.
RESUMO
BACKGROUND: Esophageal cancer (ESCA) is a major cause of cancer-related mortality worldwide. Altered fatty acid metabolism is a hallmark of cancer. However, studies on the roles of fatty acid metabolism-related genes (FRGs) in ESCA remain limited. METHOD: We identified differentially expressed FRGs (DE-FRGs). Then, the DE-FRGs prognostic model was constructed and validated using a comprehensive analysis. Moreover, the correlation between the risk model and clinical characteristics was investigated. A nomogram for predicting survival was established and evaluated. Subsequently, the difference in tumor microenvironment (TME) was compared between two risk groups. The sensitivity of key DE-FRGs to chemotherapeutic interventions and their correlation with immune cells were investigated. Finally, DEGs between two risk groups were measured and the prognostic value of key DE-FRGs in ESCA was confirmed in other databases. RESULTS: A prognostic model was constructed based on seven selected DEG-FRGs. TNM staging and CD8+ T cells were significantly correlated with high-risk groups. Low-risk groups exhibited more infiltrated M0 macrophages, an activation of type II interferon (IFN-γ) responses, and were found to be more suitable for immunotherapy. Seven key DE-FRGs with prognostic value were found to be considerably influenced by different chemotherapy drugs. CONCLUSION: A prognostic model based on seven DE-FRGs may efficiently predict patient prognosis and immunotherapy response, helping to develop individualized treatment strategies in ESCA.
RESUMO
Acquired radioresistance compromises the efficacy of radiotherapy for carcinomas including esophageal cancer (EC), thus resulting in recurrence and poor survival. Recent research corroborated radiosensitive function of simvastatin in stem-like breast cancer cells. However, its role in EC radioresistance remains poorly elucidated. Here, we developed a radioresistant EC cell line Ec9706-R with higher resistance to irradiation relative to control Ec9706 cells. Intriguingly, Ec9706-R cells exhibited epithelial-mesenchymal transition (EMT) characteristics with high invasion and migration ability. Simvastatin sensitized radioresistance of Ec9706-R cells and suppressed cell proliferation, but aggravated radiation-induced apoptosis and caspase-3 activity. Furthermore, simvastatin reversed EMT and inhibited cell invasion and migration of Ec9706-R cells. Mechanism assay confirmed the activation of PI3K/AKT pathway after radiation, which was inhibited by simvastatin. After restoring this pathway by its activator, IGF-1, simvastatin-mediated radiosensitivity and EMT reversion were abrogated. Further assay substantiated the PTEN suppression after irradiation, which was elevated following simvastatin pre-treatment. Moreover, PTEN cessation attenuated the inhibitory effect of simvastatin on PI3K/AKT activation, and subsequently antagonized simvastatin-induced radiosensitivity and EMT reversion. Additionally, simvastatin aggravated radiation-mediated Ec9706-R tumor growth inhibition. Together, simvastatin inhibits the development of Ec9706-R cells by increasing radiosensitivity and reversing EMT via PTEN-PI3K/AKT pathway, implying a promising strategy against EC radioresistance.
