Spodoptera frugiperda is an agricultural pest causing substantial damage and losses to commercial crops. Sex pheromones are critical for successful mating in Lepidoptera and have been used for monitoring and control of many pest species. The sex pheromone of S. frugiperda is known, but the genes involved in its biosynthesis have not been identified. We systematically studied 99 candidate sex pheromone genes in the genome of S. frugiperda including 1 acetyl-CoA carboxylase (ACC), 11 fatty acid synthases (FASs), 17 desaturases (DESs), 4 fatty acid transport proteins (FATPs), 29 fatty acyl-CoA reductases (FARs), 17 acetyl-CoA acetyltransferases (ACTs), 5 acyl-CoA dehydrogenase (ACDs), 3 enoyl-CoA hydratases (ECHs), 3 hydroxyacyl-CoA dehydrogenases (HCDs), 6 ethyl-CoA thiolases (KCTs), and 3 acyl-CoA-binding proteins (ACBPs). Based on the comparative transcriptome results, we found 22 candidate sex pheromone biosynthesis genes predominately expressed in pheromone glands (PGs) than abdomens without PGs including SfruFAS4, SfruFATP3, SfruACD5, SfruKCT3, SfruDES2, SfruDES5, SfruDES11, SfruDES13, SfruFAR1, SfruFAR2, SfruFAR3, SfruFAR6, SfruFAR7, SfruFAR8, SfruFAR9, SfruFAR10, SfruFAR11, SfruFAR14, SfruFAR16, SfruFAR29, SfruACT6, and SfruACT10. A combination of phylogenetic and tissue-specific transcriptomic analyses indicated that SfruDES5, SfruDES11, SfruFAR2, SfruFAR3, and SfruFAR9 may be key genes involved in the sex pheromone synthesis of S. frugiperda. Our results could provide a theoretical basis for understanding the molecular mechanisms of sex pheromone biosynthesis in S. frugiperda, and also provide new targets for developing novel pest control methods based on disrupting sexual communication.

Previous studies have linked blood cell traits (BCTs) to cardiovascular diseases (CVDs) risks, but the common genetic mechanisms underlying heritable phenotypes remain unclear. Our study used multiple analytical approaches including single nucleotide polymorphisms, genes, pathways, and protein targets to reveal common genetic elements. We confirmed both genome-wide and local genetic associations between BCTs and CVDs, identifying key pleiotropic loci and genes contributing to these links. Specifically, ALDH2, MAPKAPK5, and ACAD10, all located at 12q24.1, are associated with leukocyte-CVD traits. TNFSF12 at 17p13.1 and ABO at 9q34.2 correlate with platelet-CVD traits, while ZNF664 and CCDC92, also at 12q24.1, are linked to erythrocyte-CVD traits. Our findings also highlight multiple key trait-specific pathways mediating these phenotypic associations and potential therapeutic targets that may inform future clinical interventions. These insights significantly advance our understanding of the genetic interplay between BCTs and CVDs, underscoring the importance of focusing on BCTs to prevent cardiovascular conditions.

Gastric cancer (GC) is the fifth most common malignancy and the fifth highest cause of cancer-related deaths on a global scale. This study reveals that miR-106b-5p promotes malignant phenotypes in GC by targeting retinoblastoma-like protein 2 (RBL2). Using miR-106b-5p mimic/inhibitor and RBL2 overexpression plasmids in AGS/HGC-27 cells, this study demonstrates that miR-106b-5p promotes proliferation (CCK-8/clone formation) and migration/invasion (Transwell assay) and suppresses apoptosis (flow cytometry), while RBL2 rescues these effects. Luciferase assays confirm that miR-106b-5p directly binds the 3’UTR of RBL2 and western blotting demonstrates the presence of RBL2 downregulation. Animal studies further validate the tumour-promoting role of miR-106b-5p via RBL2 suppression, which suggests its therapeutic potential.

Gastric cancer (GC) remains a major global health challenge, with diverse risk factors and etiologies, strong invasiveness, and frequent diagnosis at advan