PVT1, which maps to chromosome 8q24, is a copy number amplification-associated long non-coding RNA. Overexpression of PVT1 is a powerful predictor of tumor progression and patient survival in a diverse range of cancer types. However, the association between PVT1 and hepatocellular carcinoma (HCC) remains unclear. The aim of the present study was to examine the expression pattern of PVT1, and its clinical significance in HCC. Between 2003 and 2012, reverse transcription-quantitative polymerase chain reaction was used to determine the expression levels of PVT1 in two independent cohorts: Cohort one, 58 HCC resection samples; and cohort 2, 214 HCC transplant samples. Additionally, the correlation between PVT1 expression levels and clinical parameters and outcomes was analyzed. The relative expression levels of PVT1 were significantly higher in cancerous tissues compared with the corresponding non-cancerous tissues (cohort one, P=0.0016; cohort two, P=0.0274). Furthermore, overexpression of PVT1 was associated with a higher serum α-fetoprotein expression level (P=0.011) and a higher recurrence rate (P=0.004). Kaplan-Meier analysis indicated that the patients with high PVT1 expression exhibited poor recurrence-free survival (P=0.021), and multivariate analysis demonstrated that high levels of PVT1 expression are an independent predictor for HCC recurrence (P=0.042; hazard ratio, 1.653). Thus, the high expression levels of PVT1 in HCC may serve as a novel biomarker for predicting tumor recurrence in HCC patients, and as a potential therapeutic target.
Long non-coding RNA HOTAIR exerts regulatory functions in various biological processes in cancer cells, such as proliferation, apoptosis, mobility, and invasion. We previously found that HOX transcript antisense RNA (HOTAIR) is a negative prognostic factor and exhibits oncogenic activity in hepatocellular carcinoma (HCC). In this study, we aimed to investigate the role and molecular mechanism of HOTAIR in promoting HCC cell migration and invasion. Firstly, we profiled its gene expression pattern by microarray analysis of HOTAIR loss in Bel-7402 HCC cell line. The results showed that 129 genes were significantly down-regulated, while 167 genes were significantly up-regulated (fold change >2, p < 0.05). Bioinformatics analysis indicated that RNA binding proteins were involved in this biological process. HOTAIR suppression using RNAi strategy with HepG2 and Bel-7402 cells increased the mRNA and protein expression levels of RNA binding motif protein 38 (RBM38). Moreover, the expression levels of RBM38 in HCC specimens were significantly lower than paired adjacent noncancerous tissues. In addition, knockdown of HOTAIR resulted in a decrease of cell migration and invasion, which could be specifically rescued by down-regulation of RBM38. Taken together, HOTAIR could promote migration and invasion of HCC cells by inhibiting RBM38, which indicated critical roles of HOTAIR and RBM38 in HCC progression.
Nowadays, solar energy has been considered as one of the most clean energy. And the data from literatures tell us that its main radiation bandwidth is approximate 295-2500 nm. In...
The paper proposes an ultra-narrow band graphene refractive index sensor, consisting of a patterned graphene layer on the top, a dielectric layer of SiO2 in the middle, and a bottom Au layer. The absorption sensor achieves the absorption efficiency of 99.41% and 99.22% at 5.664 THz and 8.062 THz, with the absorption bandwidths 0.0171 THz and 0.0152 THz, respectively. Compared with noble metal absorbers, our graphene absorber can achieve tunability by adjusting the Fermi level and relaxation time of the graphene layer with the geometry of the absorber unchanged, which greatly saves the manufacturing cost. The results show that the sensor has the properties of polarization-independence and large-angle insensitivity due to the symmetric structure. In addition, the practical application of testing the content of hemoglobin biomolecules was conducted, the frequency of first resonance mode shows a shift of 0.017 THz, and the second resonance mode has a shift of 0.016 THz, demonstrating the good frequency sensitivity of our sensor. The S (sensitivities) of the sensor were calculated at 875 GHz/RIU and 775 GHz/RIU, and quality factors FOM (Figure of Merit) are 26.51 and 18.90, respectively; and the minimum limit of detection is 0.04. By comparing with previous similar sensors, our sensor has better sensing performance, which can be applied to photon detection in the terahertz band, biochemical sensing, and other fields.
We proposed a four-band terahertz tunable narrow-band perfect absorber based on bulk Dirac semi-metallic (BDS) metamaterials with microstructure. The resonance frequency of the absorber can be adjusted by adjusting the Fermi level of BDS.
BackgroundMicrosatellite instability in colon cancer implies favorable therapeutic outcomes after checkpoint blockade immunotherapy. However, the molecular nature of microsatellite instability is not well elucidated.MethodsWe examined the immune microenvironment of colon cancer using assessments of the bulk transcriptome and the single-cell transcriptome focusing on molecular nature of microsatellite stability (MSS) and microsatellite instability (MSI) in colorectal cancer from a public database. The association of the mutation pattern and microsatellite status was analyzed by a random forest algorithm in The Cancer Genome Atlas (TCGA) and validated by our in-house dataset (39 tumor mutational burden (TMB)-low MSS colon cancer, 10 TMB-high MSS colon cancer, 15 MSI colon cancer). A prognostic model was constructed to predict the survival potential and stratify microsatellite status by a neural network.ResultsDespite the hostile CD8+ cytotoxic T lymphocyte (CTL)/Th1 microenvironment in MSI colon cancer, a high percentage of exhausted CD8+ T cells and upregulated expression of immune checkpoints were identified in MSI colon cancer at the single-cell level, indicating the potential neutralizing effect of cytotoxic T-cell activity by exhausted T-cell status. A more homogeneous highly expressed pattern of PD1 was observed in CD8+ T cells from MSI colon cancer; however, a small subgroup of CD8+ T cells with high expression of checkpoint molecules was identified in MSS patients. A random forest algorithm predicted important mutations that were associated with MSI status in the TCGA colon cancer cohort, and our in-house cohort validated higher frequencies of BRAF, ARID1A, RNF43, and KM2B mutations in MSI colon cancer. A robust microsatellite status–related gene signature was built to predict the prognosis and differentiate between MSI and MSS tumors. A neural network using the expression profile of the microsatellite status–related gene signature was constructed. A receiver operating characteristic curve was used to evaluate the accuracy rate of neural network, reaching 100%.ConclusionOur analysis unraveled the difference in the molecular nature and genomic variance in MSI and MSS colon cancer. The microsatellite status–related gene signature is better at predicting the prognosis of patients with colon cancer and response to the combination of immune checkpoint inhibitor–based immunotherapy and anti-VEGF therapy.
Bcl2-associated athanogene 3 (BAG3) protein is a co-chaperone of heat-shock protein (Hsp) 70 and may regulate major physiological and pathophysiological processes. However, few reports have examined the role of BAG3 in human hepatocellular carcinoma (HCC). In this study, we show that BAG3 regulates epithelial-mesenchymal transition (EMT) and angiogenesis in HCC. BAG3 was overexpressed in HCC tissues and cell lines. BAG3 knockdown resulted in reduction in migration and invasion of HCC cells, which was linked to reversion of EMT by increasing E-cadherin expression and decreasing N-cadherin, vimentin and slug expression, as well as suppressing matrix metalloproteinase 2 (MMP-2) expression. In a xenograft tumorigenicity model, BAG3 knockdown effectively inhibited tumor growth and metastasis through reduction in CD34 and VEGF expression and reversal of the EMT pathway. In conclusion, BAG3 is associated with the invasiveness and angiogenesis in HCC, and the BAG3 gene may be a novel therapeutic approach against HCC.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.