RESUMEN
Hepatocellular carcinoma is a common malignant tumor with high recurrence rate. Long non-coding RNA (lncRNA) ZNF561 antisense RNA 1 (ZNF561-AS1) functions as an oncogenic lncRNA to promote the tumorigenesis of colorectal cancer. The role of ZNF561-AS1 in hepatocellular carcinoma remains unknown. ZNF561-AS1 was elevated in hepatocellular carcinoma tissues and cells. Silence of ZNF561-AS1 reduced cell viability and inhibited the proliferation of hepatocellular carcinoma. The angiogenesis of hepatocellular carcinoma was also suppressed by loss of ZNF561-AS1 with a decrease of angiopoietin 2, fibroblast growth factor 1, and vascular endothelial growth factor. ZNF561-AS1 bind to miR-302a-3p, and decreased expression of miR-302a-3p in hepatocellular carcinoma. Moreover, miR-302a-3p reduced platelet-derived growth factor-D (PDGFD) in hepatocellular carcinoma, and inhibition of miR-302a-3p attenuated ZNF561-AS1 silence-induced decrease of PDGFD. In conclusion, silence of ZNF561-AS1 might inhibit cell proliferation and angiogenesis of hepatocellular carcinoma through downregulation of miR-302a-3p-mediated PDGFD.
Asunto(s)
Carcinoma Hepatocelular , Neoplasias Hepáticas , MicroARNs , ARN Largo no Codificante , Humanos , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/metabolismo , ARN sin Sentido/genética , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Regulación hacia Arriba , MicroARNs/genética , MicroARNs/metabolismo , Regulación Neoplásica de la Expresión Génica , Factor A de Crecimiento Endotelial Vascular/genética , Factor A de Crecimiento Endotelial Vascular/metabolismo , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/metabolismo , Proliferación Celular , Factor de Crecimiento Derivado de Plaquetas/genética , Factor de Crecimiento Derivado de Plaquetas/metabolismo , Línea Celular Tumoral , Movimiento Celular/genéticaRESUMEN
The principal motivation for this paper is to reduce stray light and line roughness in concave holographic gratings (CHG). Compared with other previously reported line-smoothing grating techniques such as dynamic-exposure near-field holography, we successfully improve the line smoothing of CHG to approximately 10 nm from 2 nm. Our method uses optimization technologies and a combination of photoresist hot-melting (PHM) and oxygen-ion ashing (OIA), thereby improving the degree of stray light before and after optimization by one order of magnitude; the level processed by OIA, PHM, and OIA successively is ${7.85} \times {{10}^{ - 5}}$7.85×10-5. Combining the two technologies, we achieve lower stray light and straighter groove lines for the concave gratings, which is more effective, easy to implement, and incurs a low cost.
RESUMEN
DNA-damage regulated autophagy modulator 1 (DRAM1) is known as a target of TP53-mediated autophagy, and has been reported to promote the migration and invasion abilities of glioblastoma stem cells. However, the precise contribution of DRAM1 to cancer cell invasion and migration, and the underlying mechanisms remain unclear. In the present study, small interfering (si)RNA or short hairpin RNA mediated knockdown of DRAM1 was performed in hepatoblastoma cells and the migration and invasion abilities were detected in vitro and in vivo. To investigate the underlying mechanisms, western blotting and immunofluorescence were used to detect the expression of autophagy-associated proteins and epithelial-mesenchymal-transition (EMT)-associated markers. The results showed that DRAM1 knockdown by specific siRNA abrogated cell autophagy, as well as inhibited the migration and invasion of HepG2 cells in Transwell assays, which may be reversed by rapamycin treatment. In addition, DRAM1 knockdown increased the expression of E-Cadherin while decreased the expression of vimentin in HepG2 cells, which was also be reversed by rapamycin treatment. Taken together, these results suggest that DRAM1 is involved in the regulation of the migration and invasion of HepG2 cells via autophagy-EMT pathway.