Dunlaplittle5270

Purpose The current study was set with a purpose to assess the regulatory role of micro RNA (miR)-138 in human lung cancer cells with emphasis on the underlying mechanism of action. Methods RT-PCR based analysis was employed for gene expression studies. MTT assay was used to determine the proliferation rates of lung cancer cells. Colony forming assay was performed for the analysis of colony forming potential. DAPI and Annexin V-FITC/propidium iodide (PI) double staining methods were performed for the analysis of apoptosis. Migration and invasion of cancer cells were assessed using wound healing and transwell assays, respectively. Dual luciferase reporter assay was performed for interactional study. Western blotting was used to determine the protein concentrations. Results Cancer cells had lower levels of miR-138 transcripts. The overexpression of miR-138 reduced the proliferation of cancer cells and cells were seen to form lower number of viable colonies. This was due to the induction of cancer cell apoptosis under miR-138 overexpression. miR-138 also inhibited the metastasis of lung cancer cells. miR-138 was found to interact with SOX4 intracellularly and SOX4 protein levels decreased under miR-138. The anticancer effects of miR-138 were shown to be modulated through SOX4. Conclusion MiRs have a potential to act as molecular markers in cancer prognosis. There is a need to screen for miRs specific to particular types of cancer and to look for their potential to function as anticancer entities at molecular level.Purpose To explore the effect of aquaporin-3 (AQP3) on the functions of lung cancer stem cells (LCSCs), and its molecular mechanism in regulating the differentiation and apoptosis of LCSCs through the Wnt/glycogen synthase kinase-3β (GSK-3β)/β-catenin pathway. Methods The stem cells were selected and the cell lines with low expression of AQP3 were constructed, followed by transcriptome sequencing. LCSCs were transfected with empty lentivirus in control group and transfected with AQP3 shRNA in interference group, and the low expression of AQP3 was inhibited using the Wnt pathway inhibitor XAV939 in interference + inhibitor group. The expressions of AQP3, Wnt/GSK-3β/β-catenin pathway genes, stemness genes, differentiation-related markers and apoptosis proteins in LCSCs were detected. Results In interference group, the pathway genes were highly expressed. The genes in interference group were enriched in the Wnt/GSK-3β/β-catenin pathway. In interference group, the expressions of β-catenin, GSK-3β and signal transducer and activator of transcription 3 (STAT3) were significantly higher, while the expression of adenomatous polyposis coli (APC) was significantly lower (p less then 0.05). The expression of Wnt5α had no difference. In interference group, the expressions of stemness-related genes were obviously higher, while the expression of CDK2 had no difference (p=0.471). Interference group had higher expressions of differentiation markers. Conclusion In conclusion, AQP3 can reduce the differentiation and inhibit the apoptosis of LCSCs through reducing the expressions of Wnt/GSK-3β/β-catenin pathway-related genes such as β-catenin, GSK-3β and STAT3, thereby affecting the tumor progression.Purpose To mine differentially expressed microRNAs (miRs) in lung adenocarcinoma (LUAD) via The Cancer Genome Atlas (TCGA). Methods The transcriptome and pathological data of LUAD patients were downloaded from TCGA. The differentially expressed genes were screened using "edgeR" package in R and analyzed by univariate and multivariate Cox regressions. The expression and clinic value of serum miR-548v in 50 patients with LUAD (study group) and 50 healthy individuals (control group) was detected by the quantitative real time polymerase chain reaction (qRT-PCR), and the diagnostic value of miR-548v in LUAD was analyzed by the receiver operating characteristic (ROC) curve. Results A total of 233 differentially expressed genes were found, of which 115 were highly expressed and 118 were lowly expressed. Multivariate Cox regression showed that hsa-mir-142 and hsa-mir-548v were independent prognostic factors for patients with LUAD. The study group showed significantly higher serum miR-548v expression than the control group (p less then 0.001). miR-548v was related to TNM staging, lymph node metastasis, and tumor size of patients (p less then 0.05). The area under the curve (AUC) of miR-548v in diagnosing LUAD was 0.960, and that in determining TNM staging, lymph node metastasis and tumor size was 0.829, 0.851 and 0.881 respectively. Conclusion Differential expression of miR-548v predicts poor prognosis of patients with LUAD and is closely related to TNM staging, lymph node metastasis and tumor size. Therefore, it is expected to be a potential diagnostic and prognostic marker for LUAD.Purpose This study aimed to explore the effect of molecular targeted therapy combined with radiotherapy on the expression and prognostic value of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) in bone metastasis of lung cancer. Methods 82 patients with bone metastases of lung cancer who underwent targeted therapy combined with radiotherapy in Hubei Cancer Hospital were regarded as the experimental group, and another 64 patients with bone metastases of lung cancer who underwent conventional radiotherapy were regarded as the control group. Serum VEGF and COX-2 levels were measured by enzyme-linked immunosorbent assay (ELISA) before and after the treatment. The efficacy and adverse reactions of both groups were compared. this website Results The levels of COX-2 and VEGF in serum of both groups were significantly lower than those before treatment (p0.05). A significant positive correlation was found between COX-2 and VEGF in serum in the two groups before and after treatment; the survival rate of COX-2 and VEGF high expression group was significantly lower than in the low expression group (p less then 0.05); ECOG score, pathological type, COX-2 and VEGF level were independent risk factors of death in the experimental group. Conclusion Targeted therapy combined with radiotherapy has a strong inhibitory effect on the expression of COX-2 and VEGF in bone metastasis of lung cancer. There was a significant positive correlation between the expression of COX-2 and VEGF, and the use of targeted therapy combined with radiotherapy can significantly improve the efficacy and quality of life and to prolong survival.