Steroidogenic Effects of Salinity Change on the Hypothalamus-Pituitary-Gonad (HPG) Axis of Male Chinese Sea Bass (Lateolabrax maculatus).

As lower vertebrates, teleost species could be affected by dynamic aquatic environments and may respond to environmental changes through the hypothalamus-pituitary-gonad (HPG) axis to ensure their normal growth and sexual development. Chinese sea bass (Lateolabrax maculatus), euryhaline marine teleosts, have an extraordinary ability to deal with a wide range of salinity changes, whereas the salinity decrease during their sex-maturation season may interfere with the HPG axis and affect their steroid hormone metabolism, resulting in abnormal reproductive functioning. To this end, in this study, 40 HPG axis genes in the L. maculatus genome were systematically characterized and their copy numbers, phylogenies, gene structures, and expression patterns were investigated, revealing the conservation of the HPG axis among teleost lineages. In addition, freshwater acclimation was carried out with maturing male L. maculatus, and their serum cortisol and 11-ketotestosterone (11-KT) levels were both increased significantly after the salinity change, while their testes were found to be partially degraded. After salinity reduction, the expression of genes involved in cortisol and 11-KT synthesis (cyp17a, hsd3b1, cyp21a, cyp11c, hsd11b2, and hsd17b3) showed generally upregulated expression in the head kidneys and testes, respectively. Moreover, cyp11c and hsd11b2 were involved in the synthesis and metabolism of both cortisol and 11-KT, and after salinity change their putative interaction may contribute to steroid hormone homeostasis. Our results proved the effects of salinity change on the HPG axis and steroidogenic pathway in L. maculatus and revealed the gene interactions involved in the regulation of steroid hormone levels. The coordinated interaction of steroidogenic genes provides comprehensive insights into steroidogenic pathway regulation, as well as sexual development, in teleost species.

Clinical and transcriptional signatures of human CD204 reveal an applicable marker for the protumor phenotype of tumor-associated macrophages in breast cancer.

BACKGROUND: Tumor-associated macrophages in human breast cancer are poorly understood. Specific tumor-associated macrophage-related molecular mechanisms among different intrinsic molecular subtypes remain unclear. Here, we have identified and explored the roles of the tumor-associated macrophages novel marker: CD204 in different subtypes of breast cancer. RESULTS: CD204 was upregulated in four subtypes of breast cancer, and this was associated with poor survival outcomes. CD204 could promote tumor cell proliferation, migration, and invasion and was involved in immune system-related pathways among all subtypes. Special pathways in each subtype were also found. High CD204 mRNA expressions were associated with high proportions of protumor immune cell populations, and most immunoinhibitors positive correlated with CD204 expression in all subtypes. CONCLUSIONS: These findings contribute to a better understanding and managing the protumor phenotype of tumor-associated macrophages in different subtypes of breast cancer. METHODS: The expression of CD204 and its clinical outcome were analyzed. The roles of CD204 in the regulation of tumor cell proliferation, migration, and invasion were studied. Potential pathways influenced by CD204 were displayed. Immune cell infiltration in different CD204 mRNA expression status and correlations between CD204 and immunoinhibitors were also analyzed.