This study examined the effects of nitrogen (N) fertilizer reduction on the carbon (C) metabolism and yield of Coreopsis tinctoria. A two-year (2020–2021) hydroponic experiment was conducted in accordance with a randomized complete group design with five N levels [0.875 mM Ca(NO3)2 (N1), 1.750 mM Ca(NO3)2 (N2), 3.500 mM Ca(NO3)2 (N3), 7.000 mM Ca(NO3)2 (N4), and 14.000 mM Ca(NO3)2 (N5)] and three replications. The results showed that low N significantly affected the functional leaf weight, C metabolism, and flower bud (or flower) numbers of C. tinctoria at harvest. Lower-N levels, especially those of the N2 treatment, significantly increased Rubisco, sucrose synthase (SS), sucrose phosphate synthase (SPS), soluble acid invertase (SAI), glucose 6-phosphate dehydrogenase (G6PDH), and 6-phosphogluconate dehydrogenase (6PGDH) activity and maintained the flower number of C. tinctoria. In addition, the balance of carbohydrates (sucrose, starch, glucose, and fructose) and ATP contents was more efficiently maintained under relatively low-N levels. These findings might suggest that reduced application of N fertilizer affects the C metabolism of leaves and maintains the number of flowers in Coreopsis tinctoria. Applying relatively low-N fertilizer levels is also a promising cultivation strategy for C. tinctoria.
分化聚类36(cluster of differentiation 36,CD36)是一种位于细胞表面的膜蛋白受体,可以结合并转运脂肪酸。内质网膜蛋白4B (Nogo-B)在肝脏中调控脂肪酸代谢而影响肝癌的发展。目前并不清楚CD36和Nogo-B的相互作用是否能够影响乳腺癌细胞的增殖和迁移。本研究在三阴性乳腺癌(triple-negative breast cancer,TNBC)细胞中同时干预CD36与Nogo-B的表达来探索它们对细胞增殖与迁移的影响。结果表明在三阴性乳腺癌细胞中,单独抑制CD36或Nogo-B的表达都能够抑制细胞的增殖与迁移;同时抑制CD36与Nogo-B的表达时,这种抑制效果更加明显,且Vimentin、B细胞淋巴瘤-2(B-cell lympoma-2,BCL2)和增殖细胞核抗原(proliferating cell nuclear antigen,PCNA)的表达受到抑制。在小鼠移植瘤模型中,E0771细胞转染CD36或Nogo-B的siRNA后成瘤能力降低;同时敲减CD36和Nogo-B时,肿瘤生长速度显著减慢。机制研究发现,抑制CD36和Nogo-B表达能够抑制脂肪酸结合蛋白4(fatty acid binding protein 4,FABP4)和脂肪酸转运蛋白4(fatty acid transport protein 4,FATP4) mRNA的含量,同时CD36和Nogo-B过表达刺激的细胞增殖被FABP4的siRNA降低,预示着抑制乳腺癌细胞中CD36与Nogo-B的表达可能通过抑制脂肪酸的吸收和转运而抑制细胞的生长和迁移。此外,抑制CD36与Nogo-B的表达可激活P53-P21-Rb信号通路,参与抑制CD36与Nogo-B表达而抑制的细胞增殖与迁移。本研究证明同时抑制CD36和Nogo-B的表达能够协同抑制三阴性乳腺癌细胞的增殖和迁移,为临床抗三阴性乳腺癌药物的开发提供了新的靶点。 相似文献