The intestinal microflora diversity of aboriginal chickens in Jiangxi province, China.

Intestinal microbiota can coevolve with host to form symbiotic relationship and be participated in the regulation of host physiological function. At present, there is no clear explanation on the effect of intestinal microflora in Jiangxi aboriginal chickens. Here, we investigated the association between gut microbiota and host genome of Jiangxi local chickens using 16S rRNA sequencing and genome-wide association studies (GWAS). The results showed that the breeds and genders had important effects on the intestinal microbiota of chickens. A total of 28 SNPs in 14 regions of the chicken genome were related to the relative abundance of microorganisms in 5 genera: Clostridium_sensu_stricto_1, Enterococcus, Gallibacterium, Turicibacter, and Rikenellaceae_RC9_gut_group. A total of 17 candidate genes were identified composition of chicken microbiome and show an association between the host genome and the chicken intestinal microbiota, which also unveiled the diversity of intestinal microbes in Jiangxi chickens. Given the correlation between chicken genome and intestinal microbe found in the present study, a new idea for the protection of aboriginal chicken genetic resources in China could be provided.

Androgen dihydrotestosterone promotes bladder cancer cell proliferation and invasion via EPPK1-mediated MAPK/JUP signalling.

The incidence of bladder cancer (BLCA) in men is higher than that in women. Differences in androgen levels between men and women are considered the main causes of incidence rate differences. In this study, dihydrotestosterone (DHT) significantly increased the proliferation and invasion of BLCA cells. In addition, BLCA formation and metastatic rates were higher in N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-treated male mice than in female and castrated male mice in vivo. However, immunohistochemistry showed that androgen receptor (AR) was expressed at low levels in normal and BLCA tissues of men and women. The classical AR pathway considers that DHT binds to AR and induces it to enter the nucleus, where it functions as a transcription factor. Here, a non-AR combination pathway of androgen that promoted BLCA development was investigated. The EPPK1 protein was bombarded with DHT, as determined by biotinylated DHT-binding pull-down experiments. EPPK1 was highly expressed in BLCA tissues, and EPPK1 knockdown significantly inhibited BLCA cell proliferation and invasion promoted by DHT. Moreover, JUP expression was elevated in DHT-treated high-EPPK1 expressing cells, and JUP knockdown inhibited cell proliferation and invasion. EPPK1 overexpression increased tumour growth and JUP expression in nude mice. Furthermore, DHT increased the expression of the MAPK signals p38, p-p38, and c-Jun, and c-Jun could bind to the JUP promoter. However, the promotion of p38, p-p38, and c-Jun expression by DHT was not observed in EPPK1 knockdown cells, and a p38 inhibitor suppressed the DHT-induced effects, indicating that p38 MAPK may be involved in the regulation of DHT-dependent EPPK1-JUP-promoted BLCA cell proliferation and invasion. The growth of bladder tumours in BBN-treated mice was inhibited by the addition of the hormone inhibitor goserelin. Our findings indicated the potential oncogenic role and mechanism of DHT in BLCA pathogenesis through a non-AR pathway, which may serve as a novel therapeutic target for BLCA.

Targeting Long Non-Coding RNA TTN-AS1 Suppresses Bladder Cancer Progression.

Background: To explore the biological and clinical effects of titin-antisense RNA1 (TTN-AS1) in bladder cancer (BC) and the association between TTN-AS1 and activating transcription factor 2 (ATF2) in BC. Methods: The Kaplan-Meier method was performed to analyze the association between the expression of TTN-AS1 and prognosis of BC patients from TCGA data set and our institution. Quantitative real-time PCR (RT-PCR) was conducted to explore the expression of TTN-AS1 between the patients who underwent TURBT and Re-TURBT. MTT, colony formation, and tumor formation assays were conducted to evaluate the effect of TTN-AS1 on the ability of proliferation in BC cell lines. Transwell assay was performed to evaluate the effect of TTN-AS1 on the ability of invasion in BC cell lines. Bioinfomatics and immunohistochemical staining was used to identify the relationship between TTN-AS1 and ATF2. Results: The higher expression of TTN-AS1 was related to poorer disease-free survival (DFS) in patients with BC. The expression of TTN-AS1 was higher in BC patients who underwent Re-TURBT compared with BC patients who underwent TURBT. Knocking down TTN-AS1 resulted in inhibiting the ability of proliferation and invasion of BC cells. ATF2 may serve as a downstream target of TTN-AS1 in BC, and the high expression of ATF2 is also related to adverse DFS. Conclusion: Our study reveals that TTN-AS1 serves as an oncogene by activating ATF2 in BC. The findings suggest that TTN-AS1 may act as a novel therapeutic target for patients with BC.

High DND1 Level Indicates a Poor Prognostic Factor in Prostate Cancer.

BACKGROUND: Dead end 1 (DND1) plays a vital role during oncogenesis and cancer progression by regulating the mRNA content via competitive combination with miRNA, but what function it exerts in prostate cancer has been unclear. The purpose of this paper is to explore the correlation between DND1 expression levels and clinical characteristics in prostate cancer (PCa) patients. MATERIALS AND METHODS: To assess the expression of DND1 in tumor specimens compared with paired paracancerous tissues, the sample from 83 patients was analyzed by immunohistochemistry. The Cancer Genome Atlas (TCGA) database was used to verify our results. Subsequently, we statistically analyzed the relationship between DND1 expression and the clinical prognosis of PCa patients. RESULTS: Compared with paracancerous tissues, DND1 has a higher expression level in prostate cancer. The overexpression of DND1 in protein level was significantly associated with the higher clinical stage (P = 0.006), ISUP grading group (P < 0.001), seminal vesicle invasion (P = 0.006), and PSA density (P = 0.002). Furthermore, the overexpression of DND1 indicates a poor clinical prognosis in prostate cancer patients. CONCLUSION: High-level expression of DND1 was associated with tumor progression and poor clinical prognosis. Hence, DND1 may become a potential prognostic biomarker for PCa.

Effects of exogenous gamma-aminobutyric acid on α-amylase activity in the aleurone of barley seeds.

Gamma-aminobutyric acid (GABA), a nonprotein amino acid, often accumulates in plants exposed to certain environmental stimuli. Previous studies indicated that a closed relationship existed between endogenous GABA and seed germination. However, there are few studies on the effect of exogenous GABA on seed germination. The objective of this study was to explore whether exogenous GABA affected α-amylase activity which the activation is an important stage in seed germination. The level of endogenous GABA in barley seeds rose gradually during germination, suggesting that endogenous GABA was involved in germination. We measured starch degradation under application of various concentration GABA and found that GABA promoted seed starch degradation with a dose-responsive effect. The relationship between GABA and α-amylase activity was investigated by treating barley aleurone with exogenous GABA. The result showed that α-amylase activity began to rise after about 24 h and reached a peak at 48 h. Molecular evidence suggested that GABA increased α-amylase gene expression. We explore the possible roles played by GABA in signal transduction.

Vasohibin-1 inhibits angiogenesis and suppresses tumor growth in renal cell carcinoma.

Vasohibin-1 (VASH1) has recently been isolated as a novel inhibitor of angiogenesis. Several studies have demonstrated that VASH1 plays important roles in tumor angiogenesis but the role of this angiogenic inhibitor in renal cell carcinoma (RCC) has not been elucidated. We previously reported that VASH1 expression is reduced and is associated with clinicopathological features in RCC. In the present study, we investigated the biological effects of VASH1 in RCC by evaluating the effects of VASH1 on cell proliferation, cell cycle distribution, cell apoptosis and cell invasion in human umbilical vein endothelial cells (HUVECs) and 786-0 cells, and evaluating the effect of VASH1 on the growth of 786-0 cells in nude mice. A pReceiver-M61-VASH1 was transfected into HUVECs and 786-0 cells, and the expression level of VASH1 protein was examined by western blotting. Cell proliferation was detected by MTT assay, and cell cycle and apoptosis of HUVECs and 786-0 cells were analyzed by flow cytometry. The invasive ability of 786-0 cells was tested by Transwell assay. Finally, nude mouse models were established to evaluate the therapeutic effect of VASH1. The pReceiver-M61-VASH1 effectively induced the expression of VASH1 in HUVECs and 786-0 cells. VASH1 overexpression effectively inhibited cell proliferation, arrested the cell cycle in the G0/G1 phase and promoted cell apoptosis of HUVECs and 786-0 cells. VASH1 overexpression effectively inhibited the subcutaneous growth of 786-0 tumors in vivo. Therefore, VASH1 is a potential molecular-targeted therapy for patients with RCC.