RESUMEN
Post-mortem aging could enhance the unique flavors of beef via several biochemical pathways. The microbiota is one of the important factors in the flavor development of aging beef, but their potential relationship has rarely been studied. This study characterized the apparent meat quality, flavor profiles, and microbial communities of beef during the different post-mortem processes, followed by the investigation of the correlations between the dominant microbiota and key volatile compounds. The results showed that wet-aged beef has a higher product yield and more stable color than dry-aged beef, as evidenced by the significantly lower value of aging loss and discoloration (ΔE). According to the odor activity value, 11 out of 65 compounds were categorized as aroma-active components, and 9 of them, including 1-pentanol, 1-octen-3-ol, hexanal, nonanal, heptanal, octanal, 2-nonenal, (E)-, 2-octenal, (E)- and 2-decenal, (E)-, were enriched in beef wet-aged for 7 d. Significant variances were found in the microbial communities of different aging beef. Of these, 20 microbiota (with 10 bacterial and 10 fungal genera) were recognized as the dominant genus. Partial least squares regression combined with a correlation network model revealed that five microbial genera, including Trichosporon, Prauserella, Rhodotorula, Malassezia, and Corynebacterium, constituted the functional microbiota responsible for flavor formation in aging beef and were positively associated with ≥7 key volatile compounds (p < 0.05, |ρ| > 0.7). This study suggests that the application of wet aging within 7 d on beef is better for meat quality and provides novel insights into the mechanisms of flavor formation in post-mortem aging beef via functional microbiota.
RESUMEN
Neuropilin 1 (NRP1) promotes tumor growth, angiogenesis, tumor migration, and invasion. Its higher expression is closely related to the metastasis and poor outcome of many cancers. We have reported that NRP1 was expressed at higher levels in highly metastatic cells in comparison to minimally metastatic cells in nasopharyngeal carcinoma (NPC). However, the role of NRP1 in NPC cell migration and invasion is still unclear, and whether it could serve as a potential therapeutic target for patients with NPC still needs further investigation. In this study, our results demonstrated that ectopic expression of NRP1 in S26 and 6-10B cells promoted cell migration and invasion via wound healing and transwell assays. In contrast, knockdown of NRP1 in HONE1, CNE1 and S18 cells through Clustered Regularly Interspaced Short Palindromic Repeats interference (CRISPRi) technology suppressed cell migration and invasion. Moreover, we found that EG00229, a small molecule inhibitor of NRP1, significantly suppressed NRP1-mediated promotion of NPC cells migration and invasion. Mechanistically, we demonstrated that NRP1 promoted migration and invasion by decreasing E-cadherin levels and increasing N-cadherin levels. Collectively, our results showed that NRP1 promotes cell migration and invasion and could function as a promising target for the future treatment of patients with NPC.
