RESUMEN
Huanglongbing (HLB), a global citrus threat, is transmitted by Diaphorina citri Kuwayama, a widespread insect pest. The disease's rapid spread and incurability necessitate efficient, sustainable control strategies. This study investigates heat shock protein 70 (HSP70) genes in D. citri, known to play a pivotal role in insect survival and stress response. The genome-wide identification, gene structure analysis, and conserved protein domain analysis of 22 HSP70 genes in D. citri were performed. Furthermore, the expression of these genes during HLB infection or developmental processes was gauged. Phylogenetic analysis revealed the functional categorization of the identified genes, while gene structure and conserved motifs offered insights into gene function. The expression analysis unveiled dynamic profiles in response to infection and across development stages, potentially aiding future targeted pest control strategies. These findings offer promising leads for the design of novel inhibitors or RNAi strategies targeting D. citri and HLB.
RESUMEN
Aim To investigate the induction of endothelial cell apoptosis and the suppression of VEGF expression in cancer cells by sodium caffeate (SCA). Methods Apoptosis of transformed human umbilical vein endothelial cells (ECV304 cell line) was detected by flow cytometry, DNA electrophoresis assay and morphological assessment. Western blotting analysis was applied for determination of VEGF expression in cancer cells. Substrate degradation by type Ⅳ collagenase was measured by zymography.ELISA was used to detect the binding of type Ⅳ collagenase with relevant monoclonal antibody. Results SCA induced ECV304 cell apoptosis in a time- and dose-dependent manner. After treatment with 100 and fluorescence and distinct changes of nuclear morphology, such as pyknosis and the occurrence of apoptotic bodies. VEGF expression in hepatoma HepG-2 cells and prostate carcinoma DU145 cells was reduced after SCA treatment. The degradation activity of type Ⅳ collagenase including MMP-2 and MMP-9 secreted by giant cell pulmonary carcinoma PG cells was inhibited by SCA in a dose-dependent manner. SCA also reduced the binding of mAb 3D6, a relevant monoclonal antibody, to type Ⅳ collagenase. Conclusion SCA can induce endothelial cell apoptosis and inhibit VEGF expression as well as type Ⅳ collagenase activity in cancer cells. SCA might be active in modulating tumor angiogenesis and the microenvironment.