Rigorous coupled-wave analysis of unilateral Smith-Purcell radiation from asymmetric resonators.

The Smith-Purcell radiation produced by electrons moving closely to a grating can be enhanced by resonances. Here, we show a method to manipulate the directionality of the resonance-enhanced radiation. Using the rigorous coupled-wave analysis method, we compare the radiation from symmetric and asymmetric gratings, showing that the enhanced Smith-Purcell radiation can become unilateral with a perturbation that breaks the structural symmetry. Our work provides an effective method for frequency-domain calculation of Smith-Purcell radiation and also an approach to realize more efficient use of the radiation.

Enhancement of Smith-Purcell radiation from cylindrical gratings by quasi-bound states in the continuum.

Smith-Purcell radiation (SPR) is an important means of generating terahertz waves, and the enhancement of SPR is an attractive topic nowadays. Inspired by the phenomenon of special SPR, where the enhancement is achieved by using a high-duty-cycle grating, we describe a new, to the best of our knowledge, but more effective approach to this challenging problem. By deriving a simple analytical solution for the SPR from an annular electron beam passing through a cylindrical metallic grating, we show that the inverse structure, a low-duty-cycle grating can exhibit rather high SPR efficiencies in the presence of quasi-bound states in the continuum (quasi-BICs). The analytical prediction is supported by particle-in-cell simulations, which show that the quasi-BICs can enhance the superradiant SPR generated by a train of electron bunches by orders of magnitude. These results present an interesting mechanism for enhancing the SPR from metallic gratings, and may find applications in terahertz free-electron lasers.

Circ_0058063 regulates CDK6 to promote bladder cancer progression by sponging miR-145-5p.

BACKGROUND: The study was aimed to investigate the influence of circ_0058063 on tumorigenesis as well as the regulatory mechanism of circ_0058063/miR-145-5p/ CDK6 pathway in bladder cancer (BC). METHODS: Bioinformatics analysis was used to screen highly expressed circle RNA (circRNA) and search its downstream microRNA (miRNA) and protein. The expression level of circRNA, miRNA, and CDK6 in BC cell lines T24 and J82 were determined by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Small interfering RNA was used to downregulate circ_0058063 expression. Cell proliferation, cell cycle, cell apoptosis, and cell migration of T24 cells and J82 cells were detected through MTT assay, flow cytometry, and wound-healing assay, respectively. The relationships among miR-145-5p, circ_0058063, and CDK6 were confirmed through dual luciferase reporter assay. In vivo experiment was also performed to explore the impact of circ_0058063/miR-145-5p/ CDK6 pathway on tumorigenesis in BALB/c nude mice. RESULTS: Circ_0058063 was significantly overexpressed in BC tissues. The downregulation of circ_0058063 impaired BC cell proliferation and migration ability but improved cell apoptosis ability. Circ_0058063 repressed miR-145-5p, which inhibited the expression of CDK6. Downregulation of circ_0058063 or miR-145-5p transfection contributed to more cells arresting in G0/G1 stage. MiR-145-5p suppressed cell growth and migration ability in BC, whereas CDK6 exerted the opposite influence on these cellular events. In vivo experiment also indicated that tumor development in BALB/c nude mice was repressed remarkably when circ_0058063 was downregulated. CONCLUSION: Circ_0058063 acted as a sponge of miR-145-5p to promote BC progression by regulating CDK6 expression, which provided some potential targets for BC treatment.

Circular RNA CEP128 promotes bladder cancer progression by regulating Mir-145-5p/Myd88 via MAPK signaling pathway.

The present experiment was designed for exploring the regulatory mechanism of circ-CEP128/miR-145-5p/MYD88 axis in bladder cancer. MiRNAs and circRNAs expression data were derived from Gene Expression Omnibus database with bladder tumor tissues and paracarcinoma tissue samples. Differentially expressed genes in tumor were analyzed via R software. Interaction network of differently expressed miRNAs and differently expressed mRNA was established by means of Cytoscape software. CircCEP128 and miR-145-5p expression levels were determined using qRT-PCR. The expression of MAPK signaling-related proteins MYD88, p38, ERK and JNK was examined by western blot. The relationship between circCEP128 and miR-145-5p was validated using RNA immunoprecipitation. The level of cell propagation and migration was determined by CCK8 and wound healing assay, 5-bromo-2'-deoxyuridine assay and migration assay. Cell apoptosis rate and cell cycle were detected via flow cytometry. Tumor xenograft assay was implemented to investigate the function of circCEP128 in vivo. CircCEP128 and MYD88 were overexpressed in bladder cancer based on microarray analysis and miR-145-5p was a potential targeting factor in bladder cancer. CircCEP128 targeted miR-145-5p and miR-145-5p targeted MYD88. Expression of miR-145-5p was decreased in cancer samples. Knockdown of circCEP128 induced the inhibition of cell viability and mobility and cell cycle arrest. Overexpression of miR-145-5p or knockdown of circCEP128 promoted MAKP signaling pathway and related proteins expression. In addition, knockdown of circCEP128 suppressed the growth of bladder cancer tumor tissues in vivo. Overexpression of circCEP128 promoted bladder cancer progression through modulating miR-145-5p and MYD88 via MAKP signaling pathway.

Transcription factor ATF3 mediates the radioresistance of breast cancer.

This study was designed to research the influence of activating transcription factor 3 (ATF3) on the radioresistance of breast cancer. ATF3 expression was measured by qRT-PCR and immunohistochemistry. Cancerous cell lines were cultured in vitro, and the expression of ATF3 was gauged by both qRT-PCR and Western blot before and after the radiation therapy. Cellular cycle and apoptosis were analysed by flow cytometry. Changes in the expression of corresponding proteins in the downstream pathways were identified by Western blot. Tumour xenograft was used to evaluate the effect of ATF3 in vivo. ATF3 was observed stronger in breast cancer tissues and cells. After radiation therapy, the expression of ATF3 in breast cancer cells was up-regulated. Silencing ATF3 could promote G2/M phase block, facilitate cell apoptosis and decrease clonogenic survival rate. The overexpression of ATF3 could curb G2/M-phase block, cell apoptosis and increase clonogenic survival rate. Overexpression ATF3 could increase radioresistance by up-regulating the level of phosphorylation of Akt in the PI3K/Akt signalling pathway. Radioresistance of breast cancer cells could be alleviated by inhibiting the PI3K/Akt signalling pathway. ATF3 could also promote radioresistance in vivo. ATF3 gene was able to promote radioresistance of breast cancer cells.

The Dysregulated Expression of KCNQ1OT1 and Its Interaction with Downstream Factors miR-145/CCNE2 in Breast Cancer Cells.

BACKGROUND/AIMS: Next-generation sequencing (NGS) has revealed abundant long noncoding RNAs (lncRNAs) that have been characterized as critical components of cancer biology in humans. The present study aims to investigate the role of the lncRNA KCNQ1OT1 in breast cancer (BRCA) as well as the underlying molecular mechanisms and functions of KCNQ1OT1 involved in the progression of BRCA. METHODS: The Cancer Genome Atlas (TCGA) and StarBase v2.0 were used to obtain the required gene data. Dual luciferase reporter gene assays were conducted to verify the relevant intermolecular target relationships. QRT-PCR and Western blot were performed to measure the expression levels of different molecules. Cell proliferation was detected by using the MTT and colony formation assays, while cell migration and invasion were examined by transwell assay. Variations in cell apoptosis and cell cycle were determined through flow cytometry. A tumor xenograft model was applied to assess tumor growth in vivo. RESULTS: KCNQ1OT1 was found to be remarkably highly expressed in BRCA tissues and cells. KCNQ1OT1 modulated CCNE2 through sponging miR-145 in BRCA. KCNQ1OT1 promoted tumor growth in vivo by regulating miR-145/CCNE2. CONCLUSION: The KCNQ1OT1/miR-145/CCNE2 axis plays a critical regulatory role in BRCA, potentially giving rise to BRCA tumorigenesis and progression. These findings provide valuable evidence for improving the diagnosis and treatment of BRCA in the future.

LncRNA PART1 modulates toll-like receptor pathways to influence cell proliferation and apoptosis in prostate cancer cells.

We investigated thoroughly the effect of lncRNA PART1 on prostate cancer cells proliferation and apoptosis, through regulating toll-like receptor (TLR) pathways. LncRNA PART1 expression was also examined by quantitative real-time polymerase chain reactions (qRT-PCR) in human tissues and the cells lines LNCaP and PC3. After transfection with si-PART1 or control constructs, the cell viability was measured by MTS and colony formation assays. In addition, the apoptosis rate of the prostate cancer cells was validated by TUNEL staining. Relationships between lncRNA PART1 expression and TLR pathway genes were demonstrated by qRT-PCR and Western blotting. High levels of lncRNA PART1 expression were correlated with advanced cancer stage and predication of poor survival. LncRNA PART1 levels was increased in PCa cells treated with 5α-dihydrotestosterone (DHT), confirming PART1 was directly induced by androgen. Moreover, down-regulation of lncRNA PART1 inhibited prostate cancer cell proliferation and accelerated cell apoptosis. In addition, lncRNA PART1 induced downstream genes expression in TLR pathways including TLR3, TNFSF10 and CXCL13 to further influence prostate cancer cells, indicating its carcinogenesis on prostate cancer. LncRNA PART1 promoted cell proliferation ability and apoptosis via the inhibition of TLR pathways in prostate cancer. LncRNA PART1 could hence be considered as a new target in the treatment of prostate cancer.

LncRNA HOTAIR influences cell growth, migration, invasion, and apoptosis via the miR-20a-5p/HMGA2 axis in breast cancer.

To study the regulatory effect of lncRNA HOTAIR/miR-20a-5p/HMGA2 axis on breast cancer (BC) cell growth, cell mobility, invasiveness, and apoptosis. The microarray data of lncRNAs and mRNAs with differential expression in BC tissues were analyzed in the Cancer Genome Atlas (TCGA) database. LncRNA HOX transcript antisense RNA (lncRNA HOTAIR) expression in BC was assessed by qRT-PCR. Cell viability was confirmed using MTT and colony formation assay. Cell apoptosis was analyzed by TdT-mediated dUTP nick-end labeling (TUNEL) assay. Cell mobility and invasiveness were testified by transwell assay. RNA pull-down and dual luciferase assay were used for analysis of the correlation between lncRNA HOTAIR and miR-20a-5p, as well as relationship of miR-20a-5p with high mobility group AT-hook 2 (HMGA2). Tumor xenograft study was applied to confirm the correlation of lncRNA HOTAIR/miR-20a-5p/HMGA2 axis on BC development in vivo. The expression levels of the lncRNA HOTAIR were upregulated in BC tissues and cells. Knockdown lncRNA HOTAIR inhibited cell propagation and metastasis and facilitated cell apoptosis. MiR-20a-5p was a target of lncRNA HOTAIR and had a negative correlation with lncRNA HOTAIR. MiR-20a-5p overexpression in BC suppressed cell growth, mobility, and invasiveness and facilitated apoptosis. HMGA2 was a target of miR-20a-5p, which significantly induced carcinogenesis of BC. BC cells progression was mediated by lncRNA HOTAIR via affecting miR-20a-5p/HMGA2 in vivo. LncRNA HOTAIR affected cell growth, metastasis, and apoptosis via the miR-20a-5p/HMGA2 axis in breast cancer.

Knockdown of fibrous sheath interacting protein 1 expression reduces bladder urothelial carcinoma cell proliferation and induces apoptosis via inhibition of the PI3K/AKT pathway.

BACKGROUND: FSIP1 plays a vital role in tumorigenesis and cancer progression. In bladder cancer, FSIP1 overexpression was associated with poor prognosis of bladder urothelial carcinoma. In this study, we investigated whether FSIP1 is essential in the progression of bladder cancer and the mechanism by which it mediates this effect. METHODS: FSIP1 expression was knocked down in bladder cancer cells using lentiviral-mediated short hairpin RNA (shRNA). FSIP1 expression was detected using Western blotting, immunohistochemistry (IHC), and quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). The effects of FSIP1 knockdown on tumor cells were assessed using colony formation, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and flow cytometry (FCM) apoptosis assays in vitro and BALB/c nude mouse xenograft model in vivo. RESULTS: The findings suggested that FSIP1 protein was highly expressed in bladder cancer cell lines. Knockdown of FSIP1 resulted in reduced tumor cell viability, cell cycle arrest at G0/G1 phase and apoptosis of bladder cancer cell lines (P<0.05). Moreover, knockdown of FSIP1 expression suppressed the tumor formation and growth of bladder cancer xenografts (P<0.05). At the gene level, knockdown of FSIP1 expression downregulated the activity of the PI3K/AKT signaling pathway. CONCLUSION: This study demonstrated that knockdown of FSIP1 suppressed bladder cancer cell malignant behaviors in vitro and in vivo through the inhibition of the PI3K/AKT signaling pathway, suggesting that targeting FSIP1 could be further evaluated as a potential therapeutic strategy in bladder cancer.

Fibrous sheath interacting protein 1 overexpression is associated with unfavorable prognosis in bladder cancer: a potential therapeutic target.

The study aimed to investigate the clinical significance of fibrous sheath interacting protein 1 (FSIP1) in bladder cancer, and its potential relevance to the survival of patients with bladder cancer. A total of 225 surgical excised-bladder cancer tissues were collected from the patients with the follow-up data >5 years. The FSIP1 expressions were assayed using immunohistochemistry. The messenger RNA (mRNA) and/or protein levels of FSIP1 in fresh bladder tumor tissues as well as bladder cancer cell lines were measured by quantitative real-time polymerase chain reaction (PCR) and Western blotting analysis. The correlation of FSIP1 expression with clinicopathological parameters was also evaluated. Western blotting analysis revealed that FSIP1 protein was detected in 94.1% (16/17) of bladder tumor specimens and in all three bladder cancer cell lines (5637, BIU-87, and T24 in particular), with significantly higher expression than those of their controls. Quantitative real-time PCR demonstrated an increased FSIP1 mRNA expression level in bladder cancer tissues than in normal adjacent tissues (P=0.012). FSIP1 overexpression showed good correlation with tumor stage and lymph node metastasis (P=0.027 and 0.000, respectively). Positive FSIP1 expression was independently associated with an unfavorable overall and disease-free survival by multivariate Cox regression (P=0.037 and 0.019, respectively). FSIP1 overexpression is associated with unfavorable prognosis in patients with bladder cancer. Thus, FSIP1 represents a potential therapeutic or predictive target for bladder cancer.