[Expression of long noncoding RNA STCAT3 in gastric cancer tissues and its effect on malignant phenotype of gastric cancer cells].

Objective: To detect the expression of long noncoding RNA(lncRNA)stomach cancer-associated transcript-3(STCAT3) in gastric cancer tissues, adjacent tissues, human gastric cancer cell lines and normal gastric epithelial cell lines, and to investigate the relationship between STCAT3 expression and clinicopathological features and malignant phenotype of gastric cancer. Methods: Quantitative fluorescent real-time polymerase chain reaction (qRT-PCR) was applied to detect the lncRNA STCAT3 expression levels in gastric cancer tissues, paired adjacent non-tumorous tissues, in order to explore the relationship between STCAT3 expression and clinicopathological features of gastric cancer. lncRNA STCAT3 low-expressing and high-expressing gastric cancer cell lines were transfected with expression plasmid to simulate gain-of-function, or interference plasmid to achieve loss-of-function. Cell proliferation was measured with CCK-8 and colony formation assay, cell migration with scratch assay, and cell invasion with Transwell migration assay. human gastric tumor were also transplanted to nude mice to detect the effect of lncRNA STCAT3 on tumorigenesis. Results: The expression of lncRNA STCAT3 was generally up-regulated in gastric cancer tissues compared with the adjacent tissues(12.55±0.16 vs 6.52±0.14), with median expression level in gastric cancer tissues being 6.03 higher (P<0.05). Meanwhile, the expression level of lncRNA STCAT3 in gastric cancer tissues was not correlated with age or gender (both P>0.05), while positively correlated with TNM stage (P<0.05). Interference of lncRNA STCAT3 expression in BGC-823 cells was found associated with significantly suppressed colony formation, proliferation, invasion, and migration (all P<0.05). Over-expression of lncRNA STCAT3 in AGS cells were also founded could promote the gastric cancer cells' proliferation, colony formation, migration, and invasion (all P<0.05). Conclusions: lncRNA STCAT3 may participate in the proliferation and invasion of gastric cancer cells, indicating that dysregulation of STCAT3 expression may play a role in occurrence and development of gastric cancer. lncRNA STCAT3 has the potential to be the biomarker of gastric cancer progression and target in treatment. The underlying mechanism is yet to be further studied.

Scaling the dynamic electron scattering in imaging the graphene sheets by the high-angle annular dark-field microscopy.

Employing the graphene sheets (GSs), the electron scattering constants are measured in the high-angle annular dark-field (HAADF) imaging by the scanning transmission electron microscopy. Single scattering is found to be dominant until the layer number of 200, complying with a simple relation of I = Io(1 - e(-tau/lambda)). The discrete layer counting of the GSs enables precise determination of incident depths. This work results values of lambda = 48.2, 61.4, 97.9 and 115.6 nm for 80, 120, 160 and 200 keV electrons, respectively. The uncertainties with the mean free paths and the cross sections are confined to 10 percent. The dependences on the electron beam energy and the collection angle are discussed based on a multislice simulation.

Transcription of promoter from the human APRIL gene regulated by Sp1 and NF-kB.

A proliferation-inducing ligand (APRIL) which stimulates the cell proliferation is abundantly expressed in colorectal cancer (CRC) tumors. In this report, the promoter region of the APRIL gene was determined and the major transcription factor was investigated for the first time. Deletion analysis of 5'-flanking region of the human APRIL gene and transient transfection revealed that a 538 bp region (from -1539 to -1001) was essential for promoter activation of the APRIL gene. The data from electrophoretic mobility shift assays (EMSA) indicated that the 538 bp promoter region was responsive to the specificity protein 1 (Sp1) and nuclear factor kappa B (NF-kB). Overexpression of Sp1 or NF-kB increased the activity of the APRIL promoter. Mithramycin A (inhibitor of Sp1) and Bay11-7082 (inhibitor of NF-kB) exhibited an inhibitory activity to APRIL promoter. Our results will benefit to the APRIL gene regulation investigation and contribute to discover new drug target for the APRIL gene therapy of CRC.