The molecules that mediate innate immunity are encoded by relatively few genes and exhibit broad specificity. Detailed annotation of the Pacific oyster (Crassostrea gigas) genome, a protostome invertebrate, reveals large-scale duplication and divergence of multigene families encoding molecules that effect innate immunity. Transcriptome analyses indicate dynamic and orchestrated specific expression of numerous innate immune genes in response to experimental challenge with pathogens, including bacteria, and a pathogenic virus. Variable expression of individual members of the multigene families encoding these genes also occurs during different types of abiotic stress (environmentally-equivalent conditions of temperature, salinity and desiccation). Multiple families of immune genes are responsive in concert to certain biotic and abiotic challenges. Individual members of expanded families of immune genes are differentially expressed under both biotic challenge and abiotic stress conditions. Members of the same families of innate immune molecules also are transcribed in developmental stage- and tissue-specific manners. An integrated, highly complex innate immune system that exhibits remarkable discriminatory properties and responses to different pathogens as well as environmental stress has arisen through the adaptive recruitment of tandem duplicated genes. The co-adaptive evolution of stress and innate immune responses appears to have an ancient origin in phylogeny.

Objectives: Epithelial-mesenchymal transition (EMT) is an important process in tumor development, and several studies suggest that the Wnt/b-catenin signal pathway may play an important role in EMT. However, there is no direct evidence showing that the Wnt/b-catenin pathway actually determines the EMT induced by an exogenous signal. Our previous research has successfully proved that overexpression of hypoxiainducible factor-1a (HIF-1a) could induce EMT in LNCaP cells, but not in PC-3. The present study aims to determine whether the signal of HIF-1a for inducing prostate cancer cells to undergo EMT might possibly pass through the Wnt/b-catenin pathway. Methods: Epithelial-mesenchymal transition associated proteins were detected in several human prostate carcinoma cell lines by Western blot, and then we distinguished the EMT positive cell lines from the EMT negative cell lines. Furthermore, we evaluated the possible correlation between potency of invasiveness and proliferation among these cell lines with different characteristics of EMT using Matrigel transwell and thiazolyl blue tetrazolium bromide (MTT) assays. Finally, the different expression of some critical proteins and genes in Wnt/b-catenin signaling pathway were analyzed by Western blot and reverse transcription-polymerase chain reaction (RT-PCR) in these cells with different characteristics of EMT. Results: Among several prostate cancer cell lines, PC-3, LNCaP and PC-3/HIF-1a are EMT negative cell lines, whereas LNCaP/HIF-1a and IA8 have undergone the EMT process. EMT positive cells (LNCaP/HIF-1a and IA8) exhibit much stronger potency of invasiveness and proliferation than those of PC-3 and LNCaP, which belong to EMT negative cells. Interestingly, although PC-3/HIF-1a had not completed the EMT process, it still displayed stronger potency of invasion and proliferation, resembling EMT positive cells. The protein expression level of total glycogensynthase kinase 3b (GSK-3b) and phospho-GSK-3b in LNCaP/HIF-1a, IA8 and PC-3/HIF-1a cells significantly decreased; however, the relative ratios of p-GSK3b/t-GSK3b in LNCaP/HIF-1a, IA8 and PC-3/HIF-1a cells were significantly higher than PC-3 and LNCaP. Consistently, b-catenin protein expression increased in LNCaP/HIF-1a and IA8 cells, but not in PC-3/HIF-1a; RT-PCR confirmed these results, except for the enhanced transcription activity of b-catenin mRNA in PC-3/HIF-1a. Conclusion: Our data suggests that activation of the Wnt/b-catenin signaling pathway correlates with the characteristic of EMT and potency of invasiveness and proliferation. This may be the critical factor that directly controls the process of EMT induced by HIF-1a in prostate cancer cells.

Asprosin is a white adipose tissue-derived hormone that increases abnormally in mammals with insulin resistance. However, the role of asprosin in polycystic ovary syndrome (PCOS), a disease partly characterized by insulin resistance, and its potential connection with type 2 diabetes mellitus (T2DM) and PCOS has not been thoroughly elucidated to date. To investigate the association of asprosin with metabolic profiles, sex-related hormones, or inflammation in females with T2DM or PCOS, plasma asprosin and metabolic indicators were measured in 66 healthy females, 53 female patients with T2DM, and 41 patients with PCOS. Spearman's correlation analysis and binary logistic regression analysis models were used. Plasma asprosin was significantly higher in T2DM females than in healthy subjects (P < 0.001) and was positively correlated with fasting blood glucose (FBG), hemoglobin A1c (HbA1c), and HOMA-IR (P < 0.05). Asprosin in PCOS subjects was also higher than in healthy subjects (P < 0.001) but lower than in T2DM subjects (P < 0.05), and it was positively correlated with FBG, HbA1c, HOMA-IR, LDL-c, APOB, APOE, and testosterone (P < 0.05). The BMI-categorized subgroups of PCOS subjects also showed correlations of asprosin with metabolic profiles and sex-related hormones. Binary logistic regression analysis revealed that plasma asprosin level acted as an independent risk factor for T2DM or PCOS. These findings suggest the correlation of plasma asprosin level with glucose metabolism, lipid metabolism, sex-related hormones, and inflammation in females, supporting asprosin as a potential predictive factor for females with metabolic-related diseases. This trial is registered with ChiCTR-ROC-17010719.