RESUMEN
BACKGROUND: Long non coding RNAs (lncRNAs) have been validated to be involved in the complicated biological processes during tumor progression. LINC01207 has been identified as an oncogene in several cancer types. However, the function of LINC01207 and its underlying molecular mechanism in gastric cancer (GC) are poorly understood. METHODS: The expression level of LINC01207, miR-1301-3p and PODXL mRNA was detected in GC tissues and cells by RT-qPCR. The level of PODXL protein was examined by western blot. Colony formation assay, EdU assay, TUNEL assay, caspase-3 activity test and transwell assays were carried out to analyze the effect of LINC01207 on GC cell proliferation, apoptosis, migration and invasion. The interaction between RNAs was confirmed by luciferase reporter assay, RNA pull-down assay and RIP assay. RESULTS: LINC01207 was expressed at high level in GC tissues and cells. Silencing of LINC01207 impaired GC cell proliferation, migration and invasion but promoted cell apoptosis. Mechanistically, LINC01207 acted as a ceRNA by sponging miR-1301-3p to upregulate PODXL. Besides, miR-1301-3p silencing or PODXL overexpression could abolish the inhibitory effect of LINC01207 knockdown on GC cell growth and migration. CCCTC-binding factor (CTCF) could transcriptionally activate LINC01207 in GC cells. CONCLUSIONS: CTCF-induced activation of LINC01207 contributes to GC progression through regulating miR-1301-3p/PODXL axis.
Asunto(s)
Carcinogénesis/genética , MicroARNs/genética , ARN Largo no Codificante/genética , Sialoglicoproteínas/genética , Neoplasias Gástricas/genética , Animales , Apoptosis , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Progresión de la Enfermedad , Regulación Neoplásica de la Expresión Génica , Humanos , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Neoplasias Gástricas/patología , Regulación hacia ArribaRESUMEN
We demonstrate that a novel photodetector is constructed by CdS/poly( p-phenylene vinylene) (PPV) homogeneous hybrid nanowire arrays via a simple template-assisted electrochemical codeposition approach. Owing to the well-matched energy levels between CdS and PPV, the recombination of photogenerated electrons and holes in CdS/PPV hybrid nanowire arrays is greatly inhibited. It is found that the homogeneous hybrid nanowire arrays exhibit remarkably enhanced photoelectric response and the ON/OFF ratio by 17 times compared to the individual CdS component. More importantly, the CdS/PPV hybrid nanowire arrays are observed with significant spectral selectivity especially for green light under 545 nm. In addition, a straight linear relationship is obtained between the ON/OFF ratios and the illumination intensities, implying that the quantitative detection of illumination intensity can be achieved. The new as-prepared homogeneous hybrid organic/inorganic semiconductor nanowire arrays have a bright prospect for applications in high-sensitivity and high-speed green photodetectors.
RESUMEN
Hematopoietic pre-B cell leukemia transcription factor interacting protein (HPIP) has been shown to play an important role in the development and progression of some cancers. However, the role of HPIP in gastric cancer (GC) is unclear. Here, we show that HPIP is upregulated in most GC patients and promotes GC cell proliferation, migration, and invasion. In GC patients, HPIP positively associates with tumor size and nodal metastasis, and negatively associates with tumor differentiation. Hematopoietic pre-B cell leukemia transcription factor interacting protein increases GC cell proliferation through activation of G1 /S and G2 /M cell cycle transitions, accompanied by a marked increase of the positive cell cycle regulators, including cyclin D1, cyclin A, and cyclin B1. Hematopoietic pre-B cell leukemia transcription factor interacting protein enhances GC cell migration and invasion, and modulates epithelial-mesenchymal transition, which plays a key role in cancer cell migration and invasion. These data underscore the critical role of HPIP in GC cell proliferation and progression and suggest that HPIP inhibition may be a useful therapeutic strategy for GC treatment.