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Studies have shown that long non‐coding RNA (lncRNA) MEG3 plays a key role in osteoporosis (OP), but its regulatory mechanism is somewhat incompletely clear. Here, we intend to probe into the mechanism of MEG3 on OP development by modulating microRNA‐214 (miR‐214) and thioredoxin‐interacting protein (TXNIP). Rat models of OP were established. MEG3, miR‐214 and TXNIP mRNA expression in rat femoral tissues were detected, along with TXNIP, OPG and RANKL protein expression. BMD, BV/TV, Tb.N and Tb.Th in tissue samples were measured. Ca, P and ALP contents in rat serum were also determined. Primary osteoblasts were isolated and cultured. Viability, COL‐I, COL‐II and COL‐Χ mRNA expression, PCNA, cyclin D1, OCN, RUNX2 and osteolix protein expresion, ALP content and activity, and mineralized nodule area of rat osteoblasts were further detected. Dual‐luciferase reporter gene and RNA‐pull down assays verified the targeting relationship between MEG3, miR‐214 and TXNIP. MEG3 and TXNIP were up‐regulated while miR‐214 was down‐regulated in femoral tissues of OP rats. MEG3 silencing and miR‐214 overexpression increased BMD, BV/TV, Tb.N, Tb.Th, trabecular bone area, collagen area and OPG expression, and down‐regulated RANKL of femoral tissues in OP rats. MEG3 silencing and miR‐214 overexpression elevated Ca and P and reduced ALP in OP rat serum, elevated osteoblast viability, differentiation ability, COL‐I and COL‐Χ expression and ALP activity, and reduced COL‐II expression of osteoblasts. MEG3 specifically bound to miR‐214 to regulate TXNIP. MEG3 silencing and miR‐214 overexpression promote proliferation and differentiation of osteoblasts in OP by down‐regulating TXNIP, which further improves OP.

Gastric carcinoma is one of the most frequently diagnosed gastrointestinal tumors. Long non-coding RNAs (lncRNAs) are broadly defined as endogenous cellular non-coding RNA molecules. Studies have demonstrated that they may be associated with human cancer progression. In the present study, the role of lncRNA-maternally expressed gene 3 (MEG3) in the progression of gastric carcinoma cells was investigated in vitro and in vivo. It was demonstrated that lncRNA-MEG3 expression was downregulated in gastric carcinoma cells compared with normal gastric cells. lncRNA-MEG3 transfection increased E-cadherin expression and markedly inhibited gastric carcinoma cell growth, migration and invasion. Flow cytometric analysis revealed that lncRNA-MEG3 transfection promoted the apoptosis of gastric carcinoma cells. Western blot analysis demonstrated that lncRNA-MEG3 transfection inhibited the expression of anti-apoptotic proteins B cell lymphoma-2 (Bcl-2) and Bcl-2-like protein 2 and increased the expression of pro-apoptotic proteins caspase-3 and caspase-9 in gastric carcinoma cells. lncRNA-MEG3 transfection upregulated the expression of epithelial marker E-cadherin and inhibited the expression of mesenchymal markers vimentin and fibronectin in gastric carcinoma cells, which suggested that lncRNA-MEG3 inhibited epithelial-mesenchymal transition (EMT), which may subsequently inhibit progression in gastric carcinoma cells. The present study also revealed that lncRNA-MEG3 transfection suppressed tumor growth mainly by decreasing the expression of vascular endothelial growth factor and increasing the expression of Bcl-2 in vivo. In conclusion, these results indicated that lncRNA-MEG3 may regulate EMT-associated signaling pathways and has the potential as a therapeutic target in gastric carcinoma.

We present here a draft genome sequence of the red jungle fowl, Gallus gallus. Because the chicken is a modern descendant of the dinosaurs and the first non-mammalian amniote to have its genome sequenced, the draft sequence of its genome—composed of approximately one billion base pairs of sequence and an estimated 20,000–23,000 genes—provides a new perspective on vertebrate genome evolution, while also improving the annotation of mammalian genomes. For example, the evolutionary distance between chicken and human provides high specificity in detecting functional elements, both non-coding and coding. Notably, many conserved non-coding sequences are far from genes and cannot be assigned to defined functional classes. In coding regions the evolutionary dynamics of protein domains and orthologous groups illustrate processes that distinguish the lineages leading to birds and mammals. The distinctive properties of avian microchromosomes, together with the inferred patterns of conserved synteny, provide additional insights into vertebrate chromosome architecture.

There are three types of metastases in ovarian cancer: lymphogenous, hematogenous, and peritoneal. Dissemination of the tumor in the peritoneum is directly related with the development of ascites and a poor prognosis. The purpose of this study is to determine changes in the methylation level of a group of long non-coding RNA (lncRNA) genes at different stages of ovarian cancer progression. The methylation level of 7 lncRNA genes ( LINC00472 , LINC00886 , MAFG-DT , SNHG1 , SNHG6 , TP53TG1 , and TUG1 ) was studied by quantitative methyl-specific PCR in 93 samples of ovarian tumors and 75 paired samples of histologically normal tissue, as well as in 29 peritoneal macroscopic metastases. Using the nonparametric Mann—Whitney test, a significant ( p <0.001) increase in the level of methylation of the LINC00886 , SNHG1 , SNHG6 , and TUG1 genes in the tumor tissue was shown. For the LINC00472 , LINC00886 , and SNHG6 genes, a significant relationship was found with the clinical stage ( p ≤0.001), as well as with the appearance of metastases for the LINC00472 ( p <0.001) and SNHG6 ( p =0.005) genes. There was a significant increase in the level of methylation of MAFG-DT and TP53TG1 ( p <0.001) genes, as well as a decrease in LINC00886 ( p =0.003) in peritoneal metastases relative to the primary focus. Methylation of the LINC00472 and SNHG6 genes can be considered as a factor in initiating ovarian cancer metastasis, and methylation of the LINC00886 , MAFG-DT , and TP53TG1 genes as a colonization factor for metastases in the peritoneum. Thus, a relationship between methylation of a group of lncRNA genes at different stages of ovarian cancer dissemination was shown, which is important for understanding the mechanisms of these processes and for developing innovative approaches to ovarian cancer therapy.

Cyanophages play important roles in regulating the population dynamics, community structure, metabolism, and evolution of cyanobacteria in aquatic ecosystems. Here, we report the genomic analysis of an estuarine cyanophage, S-CREM1, which represents a new genus of T4-like cyanomyovirus and exhibits new genetic characteristics. S-CREM1 is a lytic phage which infects estuarine Synechococcus sp. CB0101. In contrast to many cyanomyoviruses that usually have a broad host range, S-CREM1 only infected the original host strain. In addition to cyanophage-featured auxiliary metabolic genes (AMGs), S-CREM1 also contains unique AMGs, including three antitoxin genes, a MoxR family ATPase gene, and a pyrimidine dimer DNA glycosylase gene. The finding of three antitoxin genes in S-CREM1 implies a possible phage control of host cells during infection. One small RNA (sRNA) gene and three cis-regulatory RNA genes in the S-CREM1 genome suggest potential molecular regulations of host metabolism by the phage. In addition, S-CREM1 contains a large number of tRNA genes which may reflect a genomic adaption to the nutrient-rich environment. Our study suggests that we are still far from understanding the viral diversity in nature, and the complicated virus–host interactions remain to be discovered. The isolation and characterization of S-CREM1 further our understanding of the gene diversity of cyanophages and phage–host interactions in the estuarine environment.

Crustacean culture has been developing rapidly in various parts of the world. Therefore, it is important to understand their reproductive biology. Insulin-like androgenic gland hormone (IAG) secreted from the androgenic gland (AG) is widely accepted as a key regulator of sexual differentiation in male crustaceans. However, recently several sex-related genes (i.e., CFSH , DEAD-box family, Tra-2 , Sxl , Dsx , Fem-1 , Sox gene family, Foxl2 , and Dmrt gene family) have been identified via transcriptomic analysis in crustaceans, indicating that sexual differentiation in crustaceans is more complicated than previously expected. It has been found that several non-coding RNAs (i.e., miRNAs, lncRNAs, and piRNAs) and IAG receptors may be involved in the sexual development of decapods. Identification and study of the regulation mechanism of sex-related genes, non-coding RNAs, and IAG receptors will provide valuable information regarding sexual development in decapods. In this review, the roles of hormonal and genetic factors in both males and females are discussed. In males, crustacean female sex hormone (CFSH), Sxl , Dmrt gene family, Dsx , Sox gene family, GEM , Fem-1 , l-GnRH-III, and corazonin play important roles in IAG regulation in the “eyestalk-IAG-testis” endocrine axis. Unlike males, the regulation mechanism and interaction of sexual genes are relatively unknown in females. However, CFSH , IAG , Fem-1 , FAMeT , Slo , UCHLs , Erk2 , Cdc2 , EGFR , Vg , VgR , and VIH seem to play crucial roles during ovarian development. This study summarizes the available information in the field, highlights gaps, and lays the foundations for further studies and a better understanding of the regulatory mechanism of sexual development in decapods.

Background Long non‐coding RNA small nucleolar RNA host gene 16 (lncRNA SNHG16) is involved in the pathogenesis of acute ischemic stroke (AIS) through the regulation of brain endothelial cell viability, inflammation, atherosclerotic plaque formation, and neural apoptosis. This study aimed to evaluate the prognostic value of lncRNA SNHG16 in AIS patients. Methods Newly diagnosed AIS patients (N = 120) were serially recruited. Their lncRNA SNHG16 expressions in peripheral blood mononuclear cells (PBMCs) were detected by reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR); serum inflammatory cytokines and adhesion molecules were determined using enzyme‐linked immunosorbent assay (ELISA). The accumulating recurrence‐free survival (RFS) and overall survival (OS) were analyzed. Moreover, controls (N = 60) were recruited and their lncRNA SNHG16 expressions in PBMCs were detected. Results LncRNA SNHG16 was declined in AIS patients compared to controls (p < 0.001). Moreover, lncRNA SNHG16 was not related to any comorbidities in AIS patients (all p > 0.05). Interestingly, lncRNA SNHG16 was negatively related to tumor necrosis factor alpha (TNF‐α) (p < 0.001), interleukin 6 (IL‐6) (p = 0.013), and intracellular cell adhesion molecule‐1 (ICAM‐1) (p = 0.024), while positively correlated with interleukin 10 (IL‐10) (p = 0.022) in AIS patients. Besides, lncRNA SNHG16 was inversely associated with the National Institutes of Health Stroke Scale (NIHSS) score in AIS patients (p = 0.003). During the follow‐up period, in 14 (11.7%) patients occurred recurrence and 5 (4.2%) patients died. Unexpectedly, lncRNA SNHG16 was not associated with accumulating RFS (p = 0.103) or OS (p = 0.150) in AIS patients. Conclusion LncRNA SNHG16 relates to lower inflammatory cytokines, adhesion molecules, and milder disease severity, but fails to predict prognosis in AIS patients. Newly diagnosed acute ischemic stroke (AIS) patients (N = 120) were serially recruited. Their long non‐coding RNA small nucleolar RNA host gene 16 (lncRNA SNHG16) expressions in peripheral blood mononuclear cells (PBMCs) were detected by reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR); serum inflammatory cytokines and adhesion molecules were determined using enzyme‐linked immunosorbent assay (ELISA). Moreover, 60 controls were recruited and their lncRNA SNHG16 expressions in PBMCs were detected. LncRNA SNHG16 was declined in AIS patients compared to controls. Interestingly, lncRNA SNHG16 was negatively related to tumor necrosis factor alpha (TNF‐α), interleukin 6 (IL‐6), and intracellular cell adhesion molecule‐1 (ICAM)‐1, while positively correlated with interleukin 10 (IL‐10) in AIS patients. Besides, lncRNA SNHG16 was inversely associated with the National Institutes of Health Stroke Scale (NIHSS) score in AIS patients. Unexpectedly, lncRNA SNHG16 was not associated with accumulating recurrence‐free survival (RFS) or overall survival (OS) in AIS patients.

Long non-coding RNAs (lncRNAs) are involved in the pathogenesis of prostate cancer (PCa) as competitive endogenous RNA. The present study aimed to investigate the molecular mechanisms of lncRNA small nucleolar RNA host gene 16 (SNHG16) in the proliferation and metastasis of PCa cells. Cancer tissues and adjacent normal tissues were collected from 80 patients with PCa who did not receive any treatment. Reverse transcription-quantitative PCR analysis was performed to detect the expression levels of SNHG16, hsa-microRNA (miRNA/miR)-373-3p and transforming growth factor-β receptor type 2 (TGF-β-R2), and Spearman's correlation coefficient analysis was performed to assess the correlations between these molecules. Furthermore, the effects of SNHG16 knockdown and overexpression on the biological functions of DU-145 PCa cells and TGF-β-R2/SMAD signaling were analyzed. The dual-luciferase reporter assay was performed to assess the associations between SNHG16 and miR-373-3p, and TGF-β-R2 and miR-373-3p, the effects of which were verified via rescue experiments. The results demonstrated that the expression levels of SNHG16 and TGF-β-R2 were significantly upregulated in PCa tissues, whereas miR-373-3p expression was significantly downregulated (P<0.001). In addition, negative correlations were observed between SNHG16 and miR-373-3p (rho, −0.631) and miR-373-3p and TGF-β-R2 (rho, −0.516). Overexpression of SNHG16 significantly promoted the proliferation, migration and invasion of PCa cells (P<0.05), and significantly increased the protein expression levels of TGF-β-R2, phosphorylated (p)-SMAD2, p-SMAD3, c-Myc and E2F4 (P<0.001). Notably, the results revealed that miR-373-3p is a target of SNHG16, and miR-373-3p knockdown rescued short hairpin (sh)-SNHG16-suppressed cellular functions by promoting TGF-β-R2/SMAD signaling. The results also revealed that miR-373-3p targets TGF-β-R2. Notably, transfection with miR-373-3p inhibitor rescued sh-TGF-β-R2-suppressed cell proliferation and migration. Taken together, the results of the present study suggest that SNHG16 promotes the proliferation and migration of PCa cells by targeting the miR-373-3p/TGF-β-R2/SMAD axis.

—Breast cancer is the most common type of cancer among women. The study of the mechanisms of metastasis, the main cause of death from breast cancer, as well as the search for new markers for early diagnosis and prognosis of breast cancer, is an extremely topical issue. New perspectives in the diagnosis and treatment of breast cancer are opened by the mechanisms of gene regulation involving non-coding RNAs, in particular, long non-coding RNAs (lncRNAs). In this work, we analyzed the methylation levels of seven lncRNA genes ( MEG3 , SEMA3B-AS1 , HAND2-AS1 , KCNK15-AS1 , ZNF667-AS1 , MAGI2-AS3 , and PLUT ) by quantitative methyl-specific PCR on a set of 79 paired (tumor/normal) samples of breast cancer. Hypermethylation of all seven lncRNA genes was revealed, and hypermethylation of HAND2-AS1 , KCNK15-AS1 , MAGI2-AS3 , and PLUT was detected in breast cancer for the first time. It was found that the level of methylation of the studied lncRNA genes correlated statistically significantly with the stage of the tumor process, the size of the tumor, and the presence of metastases in the lymph nodes. Thus, methylation of the seven studied lncRNA genes is associated with the development and progression of breast cancer, and these genes can be useful as potential markers in the diagnosis and prognosis of breast cancer.

Numerous studies have reported that the long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6; ENSG00000245910) participates in the development of malignant tumors. However, the underlying mechanism of SNHG6 in the development of melanoma remains unknown. Thus, the present study aimed to investigate the biological role of SNHG6 in the progression of melanoma. SNHG6 expression in melanoma tissues and cells was assessed using a bioinformatics approach and reverse transcription-quantitative PCR analysis. Cell viability was determined using the Cell Counting Kit-8 and colony formation assays. The correlation between microRNA (miR)-101-3p, SNHG6 and RAP2B expression levels was assessed using Pearson's correlation analysis. Bioinformatic analysis and luciferase reporter assay were utilized to confirm the interaction between miR-101-3p and SNHG6 or RAP2B. The Transwell assay was conducted to examine the migratory and invasive activities of melanoma cells. In the present study, SNHG6 expression was upregulated in melanoma tissues and cell lines, and SNHG6 silencing suppressed melanoma cell viability, migration and invasion. SNHG6 was directly bound to miR-101-3p, which interacted with RAP2B. In addition, miR-101-3p expression was negatively correlated with SNHG6 or RAP2B expression. miR-101-3p silencing partially abrogated the suppressive effect of SNHG6-knockdown on RAP2B expression. Moreover, the data demonstrated that RAP2B overexpression reversed the inhibitory effects on melanoma cell proliferation, migration and invasion induced by SNHG6 silencing. In conclusion, the present study identified that SNHG6 accelerated melanoma progression via regulating the miR-101-3p/RAP2B axis. Thus, the SNHG6/miR-101-3p/RAP2B signaling pathway may be a novel therapeutic target for melanoma.