Objective To investigate the regulating effect of Notch-1 on retinal progenitor cells (RPC) differentiating into retinal ganglion cells (RGC). Methods RPC of 14-day embryonic SD rats were induced and differentiated in the culture medium with Notch-1 antisense oligonucleotides (experimental group) or missense oligonucleotides (control group) for 14 days. The condition of growth and differentiation of the cells were observed daily under the phase-contrast microscope. RGC were identified by Thy1.1 immunocytochemistry methods and the cellular number was counted. Results RPC in both of the two groups differentiated into various retinal cells, including Thy1.1-positive RGC. The percentage of RGC derived from RPC was 31.19%plusmn;6.90% in experimental group and 16.57%plusmn;4.31% in control group, and the difference was statistically significant (t=9.84,Plt;0.001). Conclusion Notch-1 may down-regulate the differentiation of RPC, and the inhibition of Notch-1 may promote RPC differentiating into RGC. (Chin J Ocul Fundus Dis, 2007, 23: 101-103)
ObjectiveTo explore the mechanism by which LINC00636 promotes the proliferation and metastasis of non-small cell lung cancer (NSCLC) by targeting NM23-H1. MethodsBased on the Affymetrix® GeneChip Human Transcriptome Array 2.0 (HTA2.0), differentially expressed long non-coding RNA (lncRNA) in three pairs of NSCLC tissues with and without lymph node metastasis were analyzed, and LINC00636 was selected as the candidate gene. The effects of LINC00636 knockdown and overexpression on the proliferation, apoptosis, migration and subcutaneous tumorigenicity of PC9 cells were analyzed. The dual-luciferase assay was used to analyze the targeting regulation of LINC00636 on NM23-H1. ResultsThe expression of LINC00636 in the serum and tissues of NSCLC patients with lymph node metastasis was higher than that in patients without lymph node metastasis. LINC00636 knockdown could inhibit the invasion and proliferation of NSCLC cells. LINC00636 could target and regulate the expression of NM23-H1, and the expression of LINC00636 and NM23-H1 in NSCLC tissues and cells was negatively correlated. The inhibitory effect of NM23-H1 on the proliferation and invasion of PC9 cells could be partially reversed by LINC00636 overexpression. ConclusionLINC00636 promotes the proliferation and metastasis of NSCLC cells by inhibiting the expression of NM23-H1 and is a potential prognostic marker and therapeutic target for NSCLC.