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It was identified that miR‑369 was expressed at a relatively high level in the CAFs‑EVs. Neurofibromin‑1 (NF1) was hypothesized as a direct target of miR‑369 in LUSC. VX970 Also, the overexpression of miR‑369 activated the mitogen‑activated protein kinase signaling pathway by interacting with NF1, consequently potentiating LUSC cell growth. The present study provided novel insights into the action of miR‑369 in CAFs‑EVs in controlling LUSC cell migration, invasion and tumorigenesis, and identified miR‑369 in CAFs‑EVs as an important prognostic marker and therapeutic target.Systemic lupus erythematosus (SLE) is an autoimmune disorder; however, the pathogenesis is not fully understood. Accumulating evidence suggested an important role of microRNAs (miRNA/miR) in autoimmunity. The present study aimed therefore to determine the miRNA expression patterns in the B cells from the peripheral blood of 66 patients with SLE and 10 healthy controls (HCs) by using an Affymetrix GeneChip® miRNA 2.0 array. In addition, next‑generation sequencing was used to obtain the peripheral blood mononuclear cell (PBMC) miRNA profiles from three patients with SLE and three HCs. Candidate miRNAs that were considered to contribute to the pathogenesis of SLE were obtained based on the intersection of miRNA profiles. The analysis revealed a significant downregulation in miR‑29a expression levels in B cells from patients with SLE, which was subsequently verified using reverse transcription‑quantitative PCR. Based on these results, the expression pattern of miR‑29a in SLE was further investigated and its role t for treatment.Increasing evidence suggests that T‑cell immunoglobulin and mucin domain 3 (TIM‑3) displays anti‑atherosclerotic effects, but its role in vascular smooth muscle cells (VSMCs) has not been reported. The present study aimed to investigate the function of TIM‑3 and its roles in human artery VSMCs (HASMCs). A protein array was used to investigate the TIM‑3 protein expression profile, which indicated that TIM‑3 expression was increased in the serum of patients with lower extremity arteriosclerosis obliterans disease (LEAOD) compared with healthy individuals. Immunohistochemistry and western blotting of arterial tissue further revealed that TIM‑3 expression was increased in LEAOD artery tissue compared with normal artery tissue. Additionally, platelet‑derived growth factor‑BB (PDGF‑BB) displayed a positive correlation with TIM‑3 expression in HASMCs. TIM‑3 decreased the migration and proliferation of PDGF‑BB‑induced HASMCs, and anti‑TIM‑3 blocked the effects of TIM‑3. The effect of TIM‑3 on the proliferation and migration of HASMCs was further investigated using LV‑TIM‑3‑transduced cells. The results revealed that TIM‑3 also inhibited PDGF‑BB‑induced expression of the inflammatory factors interleukin‑6 and tumor necrosis factor‑α by suppressing NF‑κB activation. In summary, the present study revealed that TIM‑3 displayed a regulatory role during the PDGF‑BB‑induced inflammatory reaction in HASMCs, which indicated that TIM‑3 may display anti‑atherosclerotic effects.The aim of the present study was to identify novel prognostic biomarkers and therapeutic targets for breast cancer; thus, genes that are frequently overexpressed in several types of breast cancer were screened. Kinesin family member 20A (KIF20A) was identified as a candidate molecule during this process. Immunohistochemical staining performed using tissue microarrays from 257 samples of different breast cancer subtypes revealed that KIF20A was expressed in 195 (75.9%) of these samples, whereas it was seldom expressed in normal breast tissue. KIF20A protein was expressed in all types of breast cancer observed. However, it was more frequently expressed in human epidermal growth factor receptor 2 (HER2)‑positive and triple‑negative breast cancer than in the luminal type. Moreover, KIF20A expression was significantly associated with the poor prognosis of patients with breast cancer. A multivariate analysis indicated that KIF20A expression was an independent prognostic factor for patients with breast cancer. The suppression of endogenous KIF20A expression using small interfering ribonucleic acids or via treatment with paprotrain, a selective inhibitor of KIF20A, significantly inhibited breast cancer cell growth through cell cycle arrest at the G2/M phase and subsequent mitotic cell death. These results suggest that KIF20A is a candidate prognostic biomarker and therapeutic target for different types of breast cancer.Oridonin, an active diterpenoid isolated from Rabdosia rubescens, has been reported to exhibit anticancer activities in several tumors. link2 The aim of the present study was to investigate the anticancer effects and molecular mechanisms of oridonin in mucoepidermoid carcinoma (MEC). Treatment with oridonin induced the apoptosis of MC‑3 and YD‑15 cell and inhibited the expression of myeloid cell leukemia‑1 (MCL‑1) through the regulation of the protein level through post‑translational regulation in these cell lines. Oridonin significantly increased the expression level of truncated Bid (t‑Bid) as a downstream target of MCL‑1 and subsequently decreased the mitochondrial membrane potential. The ectopic expression of MCL‑1 protein was sufficient to reverse the induction of apoptosis and the increased t‑Bid expression induced by oridonin in both cell lines. Taken together, these results suggest that oridonin exerts an apoptotic effect through the modulation of MCL‑1 and t‑Bid in human MEC cell lines and may thus be a potential anticancer drug candidate for the treatment of human MEC.Although advances in the prediction and management of ovarian hyperstimulation syndrome (OHSS) have been introduced, complete prevention is not yet possible. Previously, we and other authors have shown that vascular endothelial growth factor, angiopoietins (ANGPTs) and sphingosine-1-phosphate are involved in OHSS etiology. In addition, we have demonstrated that ovarian protein levels of platelet-derived growth factor (PDGF) ligands -B and -D decrease in an OHSS rat model, whilst PDGFR-β and ANGPT2 remain unchanged. In the present work, we investigated the role of PDGF-B in OHSS by evaluating ligand protein levels in follicular fluid (FF) from women at risk of developing OHSS and by using an immature rat model of OHSS. We demonstrated that PDGF-B and PDGF-D are lower in FF from women at risk of developing OHSS compared to control patients (p less then 0.05). In the OHSS rat model, PDGF-B (0.5 µg/ovary) administration decreased ovarian weight (p less then 0.05), reduced serum progesterone (p less then 0.0gies.In Arabidopsis thaliana, a mitogen-activated protein kinase pathway, MEKK1-MKK1/MKK2-MPK4, is important for basal resistance, and disruption of this pathway results in dwarf, autoimmune phenotypes. To elucidate the complex mechanisms activated by the disruption of this pathway, we have previously developed a mutant screening system based on a dwarf autoimmune line that overexpressed the N-terminal regulatory domain of MEKK1. Here, we report that the second group of mutants, smn2, had defects in the SMN2 gene, encoding a DEAD-box RNA helicase. SMN2 is identical to HEN2, whose function is vital for the nuclear RNA exosome because it provides non-ribosomal RNA specificity for RNA turnover, RNA quality control, and RNA processing. Aberrant SMN1/RPS6 transcripts were detected in smn2 and hen2 mutants. Disease resistance against Pseudomonas syringae pv. tomato DC3000 (hopA1), which is conferred by SMN1/RPS6, was decreased in smn2 mutants, suggesting a functional connection between SMN1/RPS6 and SMN2/HEN2. We produced double mutants mekk1smn2 and mpk4smn2 to determine whether the smn2 mutations suppress the dwarf, autoimmune phenotypes of the mekk1 and mpk4 mutants, as the smn1 mutations do. As expected, the mekk1 and mpk4 phenotypes were suppressed by the smn2 mutations. These results suggested that SMN2 is involved in proper function of SMN1/RPS6. The GO enrichment analysis using RNA-seq data showed that defense genes were downregulated in smn2, suggesting positive contribution of SMN2 to genome-wide expression of defense genes. In conclusion, this study provides novel insight into plant immunity via SMN2/HEN2, an essential component of the nuclear RNA exosome.Nematodes are highly abundant animals with diverse habitats and lifestyles. Some are free-living while others parasitize animals or plants, and among the latter, infection abilities change across developmental stages to infect hosts and complete life cycles. To determine the relationship between transcriptome evolution and morphological divergences among nematodes, we compared 48 transcriptomes of different developmental stages across eight nematode species. The transcriptomes were clustered broadly into embryo, larva, and adult stages, with the developmental plastic stages were separated from common larval stages within the larval branch. This suggests that development was the major determining factor after lifestyle changes such as parasitism during transcriptome evolution. Such patterns were partly accounted for by tissue-specific genes-such as those in oocytes and the hypodermis-being expressed at different proportions. Although nematodes typically have 3-5 larval stages, the transcriptomes for these stages were found to be highly correlated within each species, suggesting high similarity among larval stages across species. link3 For the Caenorhabditis elegans-C. briggsae and Strongyloides stercoralis-S. venezuelensis comparisons, we found that around 50% of genes were expressed at multiple stages, whereas half of their orthologues were also expressed in multiple but different stages. Such frequent changes in expression have resulted in concerted transcriptome evolution across adjacent stages, thus generating species-specific transcriptomes over the course of nematode evolution. Our study provides a first insight into the evolution of nematode transcriptomes beyond embryonic development.Ceratonova shasta is an important myxozoan pathogen affecting the health of salmonid fishes in the Pacific Northwest of North America. C. shasta exists as a complex of host-specific genotypes, some with low to moderate virulence, and one that causes a profound, lethal infection in susceptible hosts. High throughput sequencing methods are powerful tools for discovering the genetic basis of these host/virulence differences, but deep sequencing of myxozoans has been challenging due to extremely fast molecular evolution of this group, yielding strongly divergent sequences that are difficult to identify, and unavoidable host contamination. We designed and optimized different bioinformatic pipelines to address these challenges. We obtained a unique set of comprehensive, host-free myxozoan RNA-seq data from C. shasta genotypes of varying virulence from different salmonid hosts. Analyses of transcriptome-wide genetic distances and maximum likelihood multigene phylogenies elucidated the evolutionary relationship betwefor the development of potential therapeutics for efficient control of these parasites.
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