Detector and event visualization are essential parts of the software used in high-energy physics (HEP) experiments. Modern visualization techniques and multimedia production platforms such as Unity ...provide impressive display effects and professional extensions for visualization in HEP experiments. In this study, a method for automatic detector description transformation is presented, which can convert the complicated HEP detector geometry from GDML in offline software to 3D modeling in Unity. The method was successfully applied in the BESIII experiment and can be further developed into applications such as event displays, data monitoring, or virtual reality. It has great potential in detector design, offline software development, physics analysis, and outreach for next-generation HEP experiments as well as applications in nuclear techniques for the industry.
Full text
Available for:
EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Background There is increasing evidence in support of the role of lncRNAs in tumor cell proliferation, differentiation and apoptosis. Methods We examined the expression of the lncRNA ABHD11-AS.sub.1 ...in epithelial ovarian cancer (EOC) tissues and normal ovarian tissues by real-time quantitative PCR (qRT-PCR). After inducing ABHD11-AS.sub.1 downregulation by small interfering RNA (siRNA) or ABHD11-AS.sub.1 overexpression by plasmid transfection, we examined the EOC cell phenotypes and expression of related molecules. Results Expression of the lncRNA ABHD11-AS.sub.1 in EOC tissues was higher than that in normal ovarian tissue. It was positively associated with the tumor stage (stage I/II vs. stage III/IV), and it was lower in the well-differentiated group than in the poorly/moderately differentiated group. Overexpression of ABHD11-AS.sub.1 in the ovarian cancer cell lines A2780 and OVCAR3 promoted ovarian cancer cell proliferation, invasion and migration, and inhibited apoptosis. Silencing of ABHD11-AS.sub.1 had the opposite effect. Subcutaneous injection of tumor cells in nude mice showed that ABHD11-AS.sub.1 could significantly promote tumor growth. In addition, intraperitoneal injection of tumor cells in the nude mice resulted in an increase in the metastatic ability of the tumor. Further, overexpression of ABHD11-AS.sub.1 upregulated the expression of RhoC and its downstream molecules P70s6k, MMP2 and BCL-xL. Silencing of ABHD11-AS.sub.1 had the opposite effect. The RNA pull-down assay showed that ABHD11-AS.sub.1 can combine directly with RhoC. Silencing of RhoC was found to inhibit the cancer-promoting effects of lncRNA ABHD11-AS.sub.1. Thus, it seems that RhoC is a major target of the lncRNA ABHD11-AS.sub.1. Conclusions This is the first study to demonstrate the role of RhoC in the tumor-promoting effects of the lncRNA ABHD11-AS.sub.1. The present findings shed light on new therapeutic targets for ovarian cancer treatment. Keywords: lncRNA ABHD11-AS.sub.1, Tumor, Epithelial ovarian cancer, RhoC, Tumorigenesis and progression
Full text
Available for:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Long noncoding RNAs (lncRNAs) are RNA molecules more than 200 nucleotides in length that do not encode proteins. Recent studies have reported increasing numbers of functional lncRNAs. Maternally ...expressed gene 3 (MEG3) is a maternally imprinted gene encoding an lncRNA that plays a tumor suppressor role in various tumors. However, there has been rare report on mechanism of tumorigenesis and progression of endometrial carcinoma. In the present study, we found significantly lower MEG3 expression in endometrial carcinoma tissues than in normal endometrial tissues. MEG3 overexpression inhibited endometrial cancer cell proliferation, invasion, and metastasis; promoted apoptosis; and inhibited the activation of the phosphoinositide 3-kinase (PI3K)/m-TOR signaling pathway. RNA immunoprecipitation assay (RIP) showed that MEG3 can combine directly with PI3K. Tumor xenograft implantation in nude mice showed that MEG3 could significantly suppress tumor growth. These findings provide potential new therapeutic targets for treating endometrial cancer.
Full text
Available for:
EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
MicroRNA‐142‐3p (miR‐142‐3p) was previously investigated in various cancers, whereas, it's role in breast cancer (BC) remains far from understood. In this study, we found that miR‐142‐3p was markedly ...decreased both in cell lines and BC tumor tissues. Elevated miR‐142‐3p expression suppressed growth and metastasis of BC cell lines via gain‐of‐function assay in vitro and in vivo. Mechanistically, miR‐142‐3p could regulate the ras‐related C3 botulinum toxin substrate 1 (RAC1) expression in protein level, which simultaneously suppressed the epithelial‐to‐mesenchymal transition related protein levels and the activity of PAK1 phosphorylation, respectively. In addition, rescue experiments revealed RAC1 overexpression could reverse tumor‐suppressive role of miR‐142‐3p. Our results showed miR‐142‐3p could function as a tumor suppressor via targeting RAC1/PAK1 pathway in BC, suggesting a potent therapeutic target for BC treatment.
MiR‐142‐3p is downregulated in breast cancer (BC) tissues and cell lines. MiR‐142‐3p may act as a tumor suppressor by regulating cell proliferation, migration, invasion, angiogenesis, and epithelial‐to‐mesenchymal transition process through directly downregulation of ras‐related C3 botulinum toxin substrate 1 expression and subsequently inhibiting the activity of PAK1 phosphorylation in BC.
Full text
Available for:
BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
Highly upregulated in liver cancer (HULC) is a long noncoding RNA (lncRNA), which has recently been identified as a key regulator in the progression of hepatocellular carcinoma, gliomas and gastric ...cancer. However, its role in epithelial ovarian carcinoma (EOC) remains unknown. In this study, HULC expression was examined in EOC, borderline and benign ovarian tumors, and normal ovarian tissues by RT-PCR. Ovarian cancer cell phenotypes, as well as autophagy-associated proteins were examined after HULC overexpression or downregulation by plasmid or small interfering RNA (siRNA) transfection, respectively. LncRNA-protein interactions were examined by ribonucleoprotein immunoprecipitation (RIP) assays. We found that HULC expression levels were higher in EOC tissues than normal samples. HULC overexpression induced cell proliferation, migration, invasion, whereas reduced cell apoptosis in vitro and induced tumor growth in vivo. In contrast, downregulation of HULC by siRNA transfection reduced cell proliferation, migration and invasion, and induced cell apoptosis and autophagy. Our results showed that HULC overexpression reduced ATG7, LC3-II and LAMP1 expression, while inducing SQSTM1 (P62) and ITGB1 expression. HULC downregulation had the opposite effects. Furthermore, RIP indicated that ATG7 interacted with HULC; ATG7 downregulation also induced cell proliferation, reduced apoptosis and inhibited autophagy in vitro by reducing LC3-II and LAMP1 expression, while inducing SQSTM1 expression. Furthermore, ATG7 co-transfection with HULC reversed the oncogenic effects of HULC both in vitro and in vivo; however, downregulating ATG7 did not affect cell migration and invasive ability. We found that ITGB1 siRNA co-transfection with HULC reversed the function of HULC in inducing ovarian cancer cell migration and invasive ability. Taken together, our results show that HULC may promote ovarian carcinoma tumorigenesis by inhibiting ATG7 and inducing progression by regulating ITGB1.
Endometrial carcinoma (EC) is one of the most lethal gynecologic cancers. Patients frequently have regional or distant metastasis at diagnosis. MicroRNAs are small non-coding RNAs that participate in ...numerous biological processes. Recent studies have demonstrated that miR-505 is associated with several types of cancer; however, the expression and function of miR-505 have not been investigated in EC.
miR-505 expression in normal endometrial tissue, endometrial carcinomas were quantified by Quantitative reverse transcription PCR. The endometrial carcinoma cell lines HEC-1B and Ishikawa were each transfected with miR-505 or scrambled mimics, after which cell phenotype and expression of relevant molecules were assayed. Dual-luciferase reporter assay and a xenograft mouse model were used to examine miR-505 and its target gene TGF-α.
RT-PCR results demonstrated that miR-505 was significantly downregulated in human EC tissues compared to normal endometrial tissues. Besides, miR-505 expression was negatively associated with FIGO stage (stage I-II vs. III-IV), and lymph node metastasis (negative vs. positive). In vitro, overexpression of miR-505 significantly suppressed EC cell proliferation, increased apoptosis and reduced migratory and invasive activity. A miR-505 binding site was identified in the 3' untranslated region of TGF-α mRNA (TGFA) using miRNA target-detecting software; a dual luciferase reporter assay confirmed that miR-505 directly targets and regulates TGFA. RT-PCR and Western-blotting results indicated that overexpressing miR-505 reduced the expression of TGF-α and the TGF-α-regulated proteins MMP2, MMP9, CDK2, while induced Bax and cleaved-PARP expression in EC cells. In vivo, overexpression of miR-505 reduced the tumorigenicity and inhibited the growth of xenograft tumors in a mouse model of EC.
Taken together, this study demonstrates that miR-505 acts as tumor suppressor in EC by regulating TGF-α.
Full text
Available for:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Highlights • It’s the first demonstration that miR-490-3P may inhibit EOC tumorigenesis and progression by targeting CDK1 and other genes. • Our findings suggest that miR-490-3P might suppress ...ovarian cell proliferation. • The involvement of miR-490-3P and CDK1 in EOC provide greater insight into the molecular mechanisms in cancer aggressiveness. • Approaches aimed at overexpressing miR-490-3P may serve as a promising therapeutic strategy for treating patients with EOC.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Recently, a large number of studies have focused on the important role of long non‐coding RNAs (lncRNAs) in metabolism and development and have found that abnormal lncRNA expression is associated ...with the pathogenesis and development of many diseases. The lncRNA DLEU1 is involved in many solid tumours and haematological malignancies. However, its role in epithelial ovarian carcinoma (EOC) and the associated molecular mechanisms has not been reported. In this study, quantitative reverse transcription–PCR (qRT–PCR) demonstrated higher lncRNADLEU1 expression in EOC tissues than in normal tissues. Plasmid transfection of DLEU1 to up‐regulate its expression in the ovarian cancer cell lines A2780 and OVCAR3 increased cell proliferation, migration, and invasion, while inhibited apoptosis. Nude mouse xenograft assay demonstrated that DLEU1 overexpression promoted tumour growth in vivo. QRT–PCR showed decreased miR‐490‐3p expression, while Western blotting demonstrated increased its target genes CDK1, cyclinD1 and SMARCD1, as well as matrix metalloproteinase‐2 (MMP2), Bcl‐xL and P70S6K protein expression, respectively. Short interfering RNA silencing of DLEU1 produced opposite results, where qRT–PCR showed increased miR‐490‐3p expression. The dual‐luciferase reporter assay revealed a direct interaction between DLEU1 and miR‐490‐3p. MiR‐490‐3p plays a tumour suppressor role in epithelial ovarian cancer by targeting CDK1 regulation and influencing SMARCD1 and cyclin D1 (CCND1) expressions. Therefore, we suggest that through interaction with miR‐490‐3p, DLEU1 may influence the expression of CDK1, CCND1 and SMARCD1 protein, subsequently promoting the development and progression of EOC.
Full text
Available for:
FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
Skeletal aging is characterized by low bone turnover and marrow fat accumulation. However, the underlying mechanism for this imbalance is unclear. Here, we show that during aging in rats and mice ...proinflammatory and senescent subtypes of immune cells, including macrophages and neutrophils, accumulate in the bone marrow and secrete abundant grancalcin. The injection of recombinant grancalcin into young mice was sufficient to induce premature skeletal aging. In contrast, genetic deletion of Gca in neutrophils and macrophages delayed skeletal aging. Mechanistically, we found that grancalcin binds to the plexin-b2 receptor and partially inactivates its downstream signaling pathways, thus repressing osteogenesis and promoting adipogenesis of bone marrow mesenchymal stromal cells. Heterozygous genetic deletion of Plexnb2 in skeletal stem cells abrogated the improved bone phenotype of Gca-knockout mice. Finally, we developed a grancalcin-neutralizing antibody and showed that its treatment of older mice improved bone health. Together, our data suggest that grancalcin could be a potential target for the treatment of age-related osteoporosis.
Display omitted
•In aging, senescent immune cells accumulate in the bone marrow and secrete grancalcin•Grancalcin represses osteogenesis and promotes adipogenesis via plexin-b2 in BMSCs•Genetic deletion of Gca in neutrophils and macrophages slows skeletal aging•Grancalcin-neutralizing antibody treatment improves skeletal health during aging
Aging is marked by reduced osteogenesis and increased adipogenesis of bone marrow stromal cells, leading to bone fragility. Here, Li et al. show that senescent immune cells contribute to this process by accumulating in the bone marrow, where they secrete the protein grancalcin, which suppresses bone turnover and promotes marrow fat accumulation.
Full text
Available for:
GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Maternally expressed gene 3 (Meg3), a long non-coding RNA, has been reported to be associated with the pathogenesis of multiple malignancies. However, little is known regarding the role of Meg3 in ...epithelial ovarian cancer (EOC). In this study, we found that the expression of Meg3 was lower in epithelial ovarian carcinoma, and has potential to be considered as a biomarker for ovarian cancer. After transfecting the ovarian cancer cell lines OVCAR3 and A2780 with Meg3, phenotypic changes and autophagy-related molecules were examined. Upregulation of Meg3 inhibited cell proliferation, plate colony formation, induced cell cycle arrest in G2 phases, and promoted apoptosis. Observation of autophagosomes was performed by transmission electron microscopy. The expression levels of LC3-II, ATG3, LAMP1 were elevated, while SQSTM1/p62 expression declined. Upregulated expression of Meg3 also suppressed tumorigenesis in vivo in a xenograft mouse model through upregulating ATG3 expression. RIP (ribonucleoprotein immunoprecipitation) and RNA pull-down assays showed that Meg3 was co-immunoprecipitated with ATG3. In addition, Meg3 protected ATG3 mRNA from degradation following treatment with actinomycin D. Overall, our results suggest that the lncRNA Meg3 acts as a tumor suppressor in EOC by regulating ATG3 activity and inducing autophagy.
PDF
