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Efficacy as well as basic safety of photodynamic treatments mediated by 5-aminolevulinic acid for the cervical intraepithelial neoplasia A couple of: A new single-center, potential, cohort review.
RESULTS Circ_0012673 was overexpressed in lung cancer tissues and cell lines. Combretastatin A4 Loss-of-functional experiment confirmed that knockdown of circ_0012673 constrained proliferation, motility and Epithelial-Mesenchymal Transition (EMT), but induced apoptosis by targeting miR-320a. Furthermore, LIMK1 was a target of miR-320a in lung cancer cells. Elevated LIMK1 could abolish the overexpression of miR-320a induced effects on lung cancer cells. Mechanistically, circ_0012673 contributed to lung cancer progression through mediating miR-320a /LIMK1 pathway. CONCLUSIONS Circ_0012673 was a tumor-promoter in lung cancer via acting as competing endogenous RNA to regulate LIMK1 expression by binding miR-320a.OBJECTIVE Transmembrane-4-L- Six-Family-1 (TM4SF1) has been found involved in the development and progression of tumor. This study aims to investigate the effect of TM4SF1 on the proliferation, migration, and invasion of non-small cell lung cancer (NSCLC) and reveal its underlying mechanisms. MATERIALS AND METHODS qRT-PCR, immunohistochemical analysis, and Western blot were used to evaluate the expression of TM4SF1 in human NSCLC tissues and cells. Cell proliferation was measured by CCK-8 and colony formation assay. Cell apoptosis was evaluated by flow cytometry assay. Cell migration and invasion were detected by wound healing and transwell assays. Co-immunoprecipitation (Co-IP) assay was used to examine the interactions between proteins. Expression levels of related proteins were determined by Western blot. For in vivo experiment, xenograft tumor models were used. RESULTS TM4SF1 was upregulated in NSCLC tissues and cell lines and closely correlated to survival time, tumor size, lymph node metastasis, distant metastasis, and clinical stage. Gain-of function and loss-of function experiments demonstrated the oncogenic effect of TM4SF1 on NSCLC cell proliferation, apoptosis, migration, and invasion. Notably, mechanism studies showed that TM4SF1 regulated the interaction between YAP and TEAD and the level of downstream target genes. Besides, sh-YAP or Peptide 17 treatment (YAP-TEAD protein-protein interaction inhibitor) reversed the effect of TM4SF1 on NSCLC cells. The in vivo research suggested that the knockdown of TM4SF1 inhibited the growth of xenograft tumor of NSCLC. CONCLUSIONS This is the first evidence demonstrating that TM4SF1 could promote proliferation, migration, and invasion in NSCLC, at least partially through a potential YAP-TEAD signaling pathway-dependent mechanism. This study might provide a potential therapeutic target for the treatment of NSCLC.OBJECTIVE Recent studies have revealed that long noncoding RNAs (lncRNAs) play important roles in the progression of tumorigenesis. Oral squamous cell carcinoma is a disease widely widespread all over the world. The aim of this study was to identify how lncRNA INHBA-AS1 functions in the progression of OSCC. PATIENTS AND METHODS LncRNA INHBA-AS1 expression in both OSCC cells and 48 paired tissue samples was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). The function of INHBA-AS1 was identified by the transwell assay, wound healing assay, and proliferation assay in vitro. Meanwhile, the role of INHBA-AS1 was investigated through tumor formation assay in vivo. Furthermore, the underlying mechanism was explored by the luciferase assays and RNA immunoprecipitation assay (RIP). RESULTS INHBA-AS1 was highly expressed in OSCC tissues when compared with adjacent tissue samples. The proliferation, invasion, and migration of OSCC cells were significantly inhibited after the knockdown of INHBA-AS1 in vitro. Meanwhile, the knockdown of INHBA-AS1 remarkably inhibited tumor growth and metastasis in vivo. Besides, miR-143-3p was down-regulated after the knockdown of INHBA-AS1 in vitro. The expression of miR-143-3p was negatively correlated with the expression of INHBA-AS1 in OSCC tissues. In addition, miR-143-3p was directly targeted by INHBA-AS1. CONCLUSIONS The knockdown of INHBA-AS1 repressed cell migration, invasion, and proliferation in OSCC by sponging miR-143-3p, which might offer a new therapeutic intervention for OSCC patients.OBJECTIVE Multiple studies have unveiled that long non-coding RNAs (lncRNAs) contribute to oncogenesis. LncRNA ARAP1 antisense RNA 1 (ARAP1-AS1) has been demonstrated to serve as an oncogene in bladder tumor and colorectal cancer. This study attempted to explore the correlation of ARAP1-AS1 expressions with clinical progress and prognosis in gastric cancer (GC) patients. PATIENTS AND METHODS RT-PCR was carried out to examine the levels of ARAP1-AS1 in 157 GC patients. The associations between ARAP1-AS1 expression and clinicopathologic features in GC patients were analyzed using the Chi-square test. The prognostic value of abnormally expressed ARAP1-AS1 in GC patients was further analyzed via Kaplan-Meier assays and multivariate survival assays. RESULTS The levels of ARAP1-AS1 were dramatically increased in GC samples compared with paired adjacent non-tumor specimens (p=0.01). The upregulation of ARAP1-AS1 was distinctly associated with TNM stage (p=0.010) and lymphatic metastasis (p=0.007). Further survival study revealed that patients with higher levels of ARAP1-AS1 had shorter overall survival (p=0.0020) and disease-free survival than those with lower levels of ARAP1-AS1. Finally, multivariate survival assay identified ARAP1-AS1 upregulation as an independent unfavorable prognostic factor in GC patients. CONCLUSIONS Our preliminary results identified a novel GC-related factor, ARAP1-AS1 which may be a potential prognostic biomarker for GC patients.OBJECTIVE To detect the relative expression of long intergenic non-protein coding ribonucleic acid (LINC) 01116 in gastric cancer (GC) tissues and cells and analyze the correlations of LINC01116 expression with the clinicopathologic characteristics of patients and investigate the biological functions of LINC01116 via in vitro experiments. PATIENTS AND METHODS The quantitative Real Time Fluorescence-Polymerase Chain Reaction (qRT-PCR) was applied to detect the relative expression level of LINC01116 in 73 cases of tissues and cells in GC patients. The patients were divided into LINC01116 high expression group and LINC01116 low expression group, and the correlations of LINC01116 with patient's pathological characteristics were statistically analyzed. In vitro experiments [cell counting kit-8 (CCK-8) assay, colony formation assay, and flow cytometry] were adopted to investigate the influences of LINC01116 on the biological functions of GC cells. RESULTS According to the results of qRT-PCR, the expression of LINC01116 was upregulated in 54 out of 73 cases of tissues (fold change >1), and it was upregulated in GC cells compared with that in the normal gastric mucosal epithelial cells (GES-1).
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