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Improvement and also assessment of the digital camera X-ray program to ascertain vertebral turn within teenage idiopathic scoliosis.
CONCLUSIONS Our results indicated that HOXA-AS2 could enhance the migration and invasion abilities of NSCLC by targeting miR-145-3p. Furthermore, these findings suggested that HOXA-AS2 might be a potential therapeutic target for NSCLC.OBJECTIVE Previous studies have shown the carcinogenic role of long-chain non-coding RNAs (lncRNA) TRERNA1. However, the role of TRERNA1 in non-small cell lung cancer (NSCLC) has not been reported. NG25 chemical structure This research aims to explore the regulatory effect of TRERNA1/FOXL1 axis on the malignant progression of NSCLC. PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression levels of TRERNA1 and FOXL1 in 39 pairs of tumor tissues and paracancerous ones collected from NSCLC patients. The potential relation between TRERNA1 expression and clinical indicators of NSCLC patients was analyzed. Meanwhile, expression levels of TRERNA1 and FOXL1 in NSCLC cell lines were also detected by qRT-PCR. In addition, TRERNA1 knockdown model was constructed in H358 and SPC-A1 cells. Cell counting kit-8 (CCK-8), cell colony formation assay, and flow cytometry were applied to analyze the influence of TRERNA1 on NSCLC cell biological functions. Finally, Dual-Luciferase reporter the involvement of FOXL1 in TRERNA1-regulated malignant progression of NSCLC. CONCLUSIONS LncRNA TRERNA1 was up-regulated both in NSCLC tissues and cell lines. Its level was associated with pathological stage and poor prognosis in NSCLC. In addition, lncRNA TRERNA1 could promote the malignant progression of NSCLC via modulating FOXL1.OBJECTIVE The importance of circular RNAs in malignant tumors has been well concerned nowadays. Oral squamous cell carcinoma (OSCC) is diagnosed prevalently in the world. Our study aims to uncover the potential functions of hsa_circ_0011946 in OSCC development. PATIENTS AND METHODS Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was performed to determine the level of hsa_circ_0011946 in OSCC tissues and cell lines. Hsa_circ_0011946 was knocked down in OSCC cells. Biological functions of hsa_circ_0011946 in OSCC were identified by performing cell proliferation assay, colony formation assay, wound healing assay, and transwell assay. The underlying mechanism of hsa_circ_0011946 in regulating OSCC progression was explored by RT-qPCR and Western blot assay. RESULTS Hsa_circ_0011946 was highly expressed in OSCC tissues compared with adjacent samples. It was also upregulated in OSCC cell lines. The knockdown of hsa_circ_0011946 inhibited cell growth, migration, and invasion in OSCC. The expression of PCNA was reduced via knockdown of hsa_circ_0011946. Furthermore, the expression of PCNA in tumor tissues was positively correlated to the expression of hsa_circ_0011946. CONCLUSIONS Hsa_circ_0011946 could promote cell growth, migration, and invasion of OSCC by upregulating PCNA, which may offer a new therapeutic intervention for OSCC patients.OBJECTIVE Currently, the importance of circular RNAs in malignant tumors has attracted much attention. However, the role of circPSMC3 in nasopharyngeal carcinoma (NPC) remains unclear. The aim of this study was to investigate the function of circPSMC3 in the proliferation and apoptosis of NPC and to explore its possible underlying mechanism. PATIENTS AND METHODS Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to determine the level of circPSMC3 in NPC tissues and cell lines. The association between circPSMC3 expression and patients' prognosis was analyzed. CircPSMC3 lentivirus was constructed and transfected into NPC cells. Cell growth ability and apoptosis were detected through Cell Counting Kit-8 (CCK-8) assay, colony formation assay, and flow cytometry, respectively. Western blot was performed to analyze the target protein of circPSMC3. Furthermore, the function of circPSMC3 was explored in nude mice. RESULTS CircPSMC3 was lowly expressed in NPC tissues compared with adjacent normal tissues. Low circPSMC3 expression was associated with poor prognosis of NPC patients. Meanwhile, the expression of circPSMC3 was significantly down-regulated in NPC cell lines as well. The growth ability of NPC cells was markedly inhibited after circPSMC3 was overexpressed. Overexpression of circPSMC3 significantly promoted the apoptosis of NPC cells in vitro. ROCK1 expression decreased markedly via overexpression of circPSMC3. Furthermore, tumor formation was inhibited after the up-regulation of circPSMC3 in vivo. CONCLUSIONS CircPSMC3 could suppress cell growth and promote cell apoptosis in NPC by downregulating ROCK1.OBJECTIVE This study aimed to clarify the impact of delayed adjuvant therapy on the outcome of HPV associated oropharyngeal squamous cell carcinoma (HPV-OPSCC). PATIENTS AND METHODS A total of 157 patients with HPV-OPSCC treated by surgery and adjuvant radiotherapy or chemoradiation therapy were analyzed retrospectively. We divided participants into two groups implementing adjuvant therapy within or after 50 days. Primary endpoints were the rates of locoregional recurrence and distant metastases, overall survival, and disease-specific survival. RESULTS Adjuvant treatment began within 50 days (average 38.8 days) in 79 cases compared to 78 cases after 50 days (average 71.5 days). Five-year overall survival was 85.7% and 87.4% (p=0.588), the rates of local and regional recurrence were 3.8% and 6.4% (p=0.455) and of distant metastases 5.1% and 9% (p=0.369) implementing adjuvant treatment within or later than 50 days, respectively. CONCLUSIONS These results suggest that adjuvant therapy initiated later than seven weeks after primary ablative surgery may still be effective HPV-OPSCC.OBJECTIVE Esophageal squamous cell carcinoma (ESCC) is the main type of esophageal cancer and is a devastating malignancy. Recent research shows that microRNA-429 (miR-429) has a role in suppressing cell proliferation, cell cycle and promoting apoptosis in many cancers. This study aims to explore the great role of miR-429 in esophageal squamous cell carcinoma. MATERIAL AND METHODS The mRNA and protein levels of miR-429 and genes were calculated by using Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) and Western blot. We applied Cell Counting Kit-8 (CCK-8) and transwell assays to measure the proliferative and migratory abilities. Meanwhile, the Kaplan-Meier method was used to calculate the overall survival of esophageal squamous cell carcinoma patients. RESULTS MiR-429 was downregulated while RAB23 was upregulated in ESCC tissues and cell lines, and downregulation of miR-429 predicted poor prognosis in ESCC. RAB23 was found to be a direct target gene of miR-429 and its expression was regulated by miR-429 in ESCC. Moreover, miR-429 inhibited the proliferation through nuclear factor-kappa B (NF-κB) pathway and inhibited cell migration-mediated epithelial-mesenchymal transition (EMT) in TE-2 cells. In addition, overexpression of miR-429 suppressed tumor growth of ESCC in vivo. CONCLUSIONS MiR-429 inhibited the proliferation through the RAB23/NF-κB pathway and the migration-mediated EMT in ESCC. The newly identified miR-429/RAB23 axis provides novel insight into the pathogenesis of ESCC.OBJECTIVE This study explored the effect of miR-26a-5p on cell proliferation, migration, and invasion in gastric cancer by targeting COL10A1. MATERIALS AND METHODS First, differentially expressed genes were identified from microarray GSE103236 data of human gastric cancer. Then, qRT-PCR was carried out to detect the expression levels of COL10A1 and miR-26a-5p in gastric cancer cells and normal cases. The CCK-8 method was used to test cell proliferation. The colony formation assay was performed for the examination of the cell colony-forming ability, and transwell was applied for the detection of cell migration and invasion. Subsequently, the targeted relationship between miR-26a-5p and COL10A1 was identified by bioinformatics methods and further verified by Dual-Luciferase assay. The rescue experiment was finally conducted to validate the miR-26a-5p-dependent mechanism on cell proliferation, migration, and invasion via targeting COL10A1. RESULTS COL10A1 was found to be highly expressed in gastric cancer cells, while miR-26a-5p was poorly expressed. Silencing COL10A1 inhibited cell proliferation, migration, and invasion in gastric cancer. Besides, miR-26a-5p could function on gastric cancer cells by reducing COL10A1. As well, the rescue experiment suggested that the down-regulation of COL10A1 could reverse the inhibitory effect of miR-26a-5p on gastric cancer cells. CONCLUSIONS Collectively, miR-26a-5p can potentiate proliferation, migration, and invasion of gastric cancer cells by targeting COL10A1.OBJECTIVE Long non-coding RNAs (lncRNAs) have been verified to involve in the development and progression of gastric cancer (GC). However, the expression of lncRNA CHRF level in GC has not been mentioned before. Here, we focused on the function of lncRNA CHRF played in GC. PATIENTS AND METHODS A total of 103 GC tissues and paired para-tumor tissues from GC patients were collected. The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was applied to measure the lncRNA CHRF level in these samples and GC cell lines. The Wound-healing experiment, transwell assay, and Matrigel assay were employed to study the migration and invasion abilities of GC cells. The underlying molecular of lncRNA CHRF was measured using Western-blot. RESULTS LncRNA CHRF expression was significantly higher in 103 GC tissue samples compared with the adjacent para-tumor samples. In GC cells, lncRNA CHRF showed increased expression levels than the human fetal gastric epithelial cells (GES-1). Inhibition of lncRNA CHRF reduced the invasion and migration of MKN-7 cells while the over-expression of lncRNA CHRF promoted HGC-27 cells metastasis. Furthermore, we found that lncRNA CHRF could promote the progression of epithelial-mesenchymal transition (EMT) to promote the GC cell metastasis. CONCLUSIONS Our current study demonstrated that lncRNA CHRF functioned as an oncogene in GC and promoted cell invasion and migration via EMT. This might furnish a potential target for the GC biological diagnosis and therapy.OBJECTIVE The objective of this systematic review was to review the available evidence on the disparity between willingness to accept (WTA) and willingness to pay (WTP) for healthcare goods and services. METHODS A tiered approach consisting of (1) a systematic review, (2) an aggregate data meta-analysis, and (3) an individual participant data meta-analysis was used. MEDLINE, EMBASE, Scopus, Scisearch, and Econlit were searched for articles reporting both WTA and WTP for healthcare goods and services. Individual participant data were requested from the authors of the included studies. RESULTS Thirteen papers, reporting WTA and WTP from 19 experiments/subgroups, were included in the review. The WTA/WTP ratios reported in these papers, varied from 0.60 to 4.01, with means of 1.73 (median 1.31) for 15 estimates of the mean and 1.58 (median 1.00) for nine estimates of the median. Individual data obtained from six papers, covering 71.2% of the subjects included in the review, yielded an unadjusted WTA/WTP ratio of 1.
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