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Have an effect on, (group-based) emotions, as well as climatic change actions.
SNHG7 was a sponge of miR-329-3p and modulated chemosensitivity and autophagy by regulating miR-329-3p. In addition, SNHG7 upregulated MYO10 by sponging miR-329-3p. MYO10 restored the effect of miR-329-3p on cisplatin sensitivity and autophagy. Moreover, suppression of autophagy blocked SNHG7-induced cisplatin resistance. CONCLUSIONS Depletion of SNHG7 potentiated cisplatin sensitivity through inhibition of autophagy by modulating miR-329-3p/MYO10 axis, providing a new therapeutic approach to overcome cisplatin resistance in NB chemotherapy.OBJECTIVE The aim of this study was to explore the function of microRNA-548c-5p in breast cancer (BCa) and the underlying mechanism. Our findings might help to provide a theoretical basis for the diagnosis and treatment of BCa. PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the expression level of microRNA-548c-5p in BCa tumor tissues and para-cancerous tissues. The relationship between microRNA-548c-5p expression and clinical indicators of BCa was analyzed. Meanwhile, the expression of microRNA-548c-5p in the BCa cells was detected by qRT-PCR as well. MicroRNA-548c-5p overexpression and the knockdown models were constructed in BCa cell lines MCF-7 and MDA-MB-231. Subsequently, Cell Counting Kit-8 (CCK-8), colony formation and 5-ethynyl-2'-deoxyuridine (EdU) assays were performed to analyze the influence of microRNA-548c-5p on biological functions of BCa cells. Finally, the interaction between microRNA-548c-5p and Wnt/b-catenin signaling pathway was investigtor group. The rescue experiments in the cells revealed that there might be a mutual regulation between microRNA-548c-5p and Wnt1, thereby together regulating the malignant growth of BCa. CONCLUSIONS MicroRNA-548c-5p was lowly expressed in BCa tissues and cells, which was closely related to the pathological stage of BCa. In addition, microRNA-548c-5p significantly inhibited the proliferation of BCa cells via modulating Wnt/b-catenin signaling pathway.OBJECTIVE The aim of this study was to explore whether SAPCD2 can affect the proliferation of breast cancer cells through YAP/TAZ, thus promoting the development of breast cancer (BCa). PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine SAPCD2 expression level in BCa tissues collected from patients in different tumor TNM-stage. The correlation between SAPCD2 expression and clinicopathological features of patients were analyzed, and the Kaplan-Meier test was used for survival analysis. In addition, after knocking down SAPCD2 in cells, qRT-PCR and Western blot were applied to analyze the expression of the related genes and proteins, respectively. Moreover, Cell Counting Kit-8 (CCK-8) and transwell experiments were conducted to detect cell viability, migration, and invasion abilities. Furthermore, the changes in cell viability and migration and invasion abilities were examined after the simultaneous overexpression of YAP. RESULTS It was found that SAPCD2 expression levels in BCa tissues were remarkably higher than those in the normal control samples; meanwhile, patients with tumor size >3 cm or in the T3+T4 stage had a relatively higher expression of SAPCD2 than those with tumor size less then 3 cm or in T1+T2 stage. At the same time, the overall survival rate of BCa patients with highly expressed SAPCD2 was remarkably lower than that of patients in the low expression group. Moreover, it was found that the SAPCD2 level was correlated to the tumor size, TNM stage, and lymph node metastasis. After knocking down SAPCD2 in cells, cell viability, migration, and invasion abilities, as well as the YAP/TAZ protein expression levels were all found to be remarkably attenuated, which, however, were reversed after simultaneous overexpression of YAP in cells. CONCLUSIONS SAPCD2 may be able to enhance the proliferation ability of BCa cells via modulating the expression of YAP/TAZ, thereby prompting the progression of BCa.OBJECTIVE Non-small cell lung cancer (NSCLC) is one of the most common and deadly tumors in the world. LncRNA FAS-AS1 was abnormally expressed in various cancers, such as non-small cell lung cancer. However, the underlying mechanism of FAS-AS1 in NSCLC remains to be elucidated. MATERIALS AND METHODS The levels of FAS-AS1 and miR-19a-5p were measured using qRT-PCR in NSCLC cells. MTT and cell colony formation assays were performed to detect cell proliferative capacity. Transwell assay was carried out to measure cell migration and invasion. The relationship between FAS-AS1 and miR-19a-5p was confirmed using Luciferase reporter assay. Xenograft tumor experiment was conducted to detect the tumor growth in vivo. RESULTS FAS-AS1 was remarkably down-regulated in NSCLC cells. FAS-AS1 inhibited cell proliferation, migration, and invasion in NSCLC cells. Additionally, FAS-AS1 directly targeted miR-19a-5p and negatively regulated the expression of miR-19a-5p in NSCLC cells. Furthermore, FAS-AS1 overexpression restored the promotion of miR-19a-5p overexpression on proliferation, migration, and invasion of NSCLC cells. Additionally, suppression of FAS-AS1 abrogated the inhibitory effects of miR-19a-5p knockdown on the progression of NSCLC. FAS-AS1 suppressed the tumor growth in vivo. CONCLUSIONS FAS-AS1 suppressed cell proliferation, migration, and invasion by sponging miR-19a-5p in NSCLC, indicating that FAS-AS1 might be a potential biomarker and therapeutic target for NSCLC.OBJECTIVE The present studies indicate that circRNAs play pivotal roles in human cancers. Lung adenocarcinoma (LUAC), one of lung cancer types, has high metastasis rate. Herein, we focused our study on the function and mechanism of circular RNA circCRIM1 in LUAC development. PATIENTS AND METHODS Quantitative Real-time polymerase chain reaction (qRT-PCR) was performed to detect the levels of circCRIM1, miR-125b-5p, and BTG anti-proliferation factor 2 (BTG2). Transwell assay was carried out to assess cell migration and invasion. The protein levels of BTG2, EMT markers, and HK2 were measured by Western blot. Glycolysis was analyzed through determining glucose consumption and lactate production. Furthermore, the targets of circCRIM1 and miR-125b-5p were predicted and verified by starBase and the dual-luciferase reporter assay, respectively. Also, whether circCRIM1 affecting tumor growth in vivo was explored using mouse xenograft assay. RESULTS CircCRIM1 and BTG2 were downregulated, and miR-125b-5p was upregulated in LUAC tissues/cells. CircCRIM1 upregulation inhibited LUAC cell migration, invasion, epithelial-mesenchymal transition (EMT), glycolysis, and tumor growth. AZD4547 solubility dmso Moreover, circCRIM1 regulated LUAC cell development through targeting miR-125b-5p. MiR-125b-5p affected LUAC cell growth via binding to BTG2. Also, circCRIM1 promoted BTG2 expression by inhibiting miR-125b-5p expression in LUAC cells. CONCLUSIONS CircCRIM1 was lowly expressed in LUAC. Moreover, circCRIM1 functioned as a sponge of miR-125b-5p to improve BTG2 expression, thereby suppressing LUAC development. Our finding indicated that circCRIM1 could be considered as a biomarker and target for the diagnosis and therapy of LUAC patients.OBJECTIVE Circular RNAs (circRNAs) can make contributions to cell proliferation, migration and invasion in lung adenocarcinoma (LUAD). Circ_Band 4.1-like protein 2 (circ_EPB41L2) was found to have anti-tumor roles in lung cancer. Herein, we investigated the roles of circ_EPB41L2 in LUAD tumorigenicity. PATIENTS AND METHODS The expression of circ_EPB41L2, microRNA (miR)-211-5p, and Cadherin-4 (CDH4) was measured using quantitative real-time polymerase chain reaction. Western blot was used to detect the levels of CDH4, Ki67, and E-cadherin. Cell proliferation, migration and invasion were examined using 3-(4,5)-dimethylthiazol(-z-y1)-3,5-di-phenyltetrazoliumbromide (MTT) assay and transwell assay, respectively. The interaction between miR-211-5p and circ_EPB41L2 or CDH4 was confirmed by Dual-Luciferase reporter assay. In vivo experiments were conducted using the murine xenograft model. RESULTS Circ_EPB41L2 and CDH4 were down-regulated in LUAD tissues and cell lines. Overexpressed circ_EPB41L2 or CDH4 acted as a suppressor in the LUAD cell proliferation, invasion and migration in vitro. MiR-211-5p directly bound to circRNA_EPB41L2 and CDH4 3'-UTR, and circ_EPB41L2 indirectly regulated CDH4 expression by binding to miR-211-5p in LUAD cells. Furthermore, rescue assay showed circ_EPB41L2 played a protective role by repressing proliferation, migration and invasion through regulating CDH4 and miR-211-5p in LUAD cells. Besides, in vivo experiments indicated circ_EPB41L2 overexpression also inhibited tumor growth through regulating miR-211-5p and CDH4. CONCLUSIONS Circ_EPB41L2 functioned as a tumor suppressor to inhibit the proliferation, migration and invasion through regulating CDH4 by miR-211-5p in LUAD cells, suggesting a new understanding on the tumorigenesis of LUAD and novel molecular therapeutic targets.OBJECTIVE The purpose of this study was to explore the role of ANXA3 in lung cancer cell resistance to oxaliplatin (OXA). MATERIALS AND METHODS After adding different concentrations of Ox, A549, and A549/Ox cell viability were examined using cell counting kit-8 (CCK-8) assay, and the mRNA and protein expressions of ANXA3 were analyzed by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot, respectively. After treating cells with 5 μg/mL and 15 μg/mL Ox for 24 hours and knocking down ANXA3, qRT-PCR, CCK8, flow cytometry, transwell, and BrdU assays were performed to examine ANXA3 expression level, cell viability, apoptosis, migration, and proliferative capacities, respectively. In addition, Western blot was performed to detect the protein expression of c-caspase 3. RESULTS The higher the concentration of Ox added, the worse the cell viability. Meanwhile, ANXA3 expression in A549/Ox cells was found remarkably higher than that in normal A549 cells. After treated with different concentrations of Ox for 24 hours, the cell viability, migration capacity and cell proliferation of A549 cells were found remarkably decreased, while the opposite results were observed in cell apoptosis and C-caspase 3 protein expression, and the Ox treatment group was evidently lower than control group. CONCLUSIONS Knockdown of ANXA3 may be able to inhibit the resistance of LCa cells to OXA.OBJECTIVE To illustrate the role of interleukin 6 (IL-6) in the progression of non-small cell lung cancer (NSCLC) via activating STAT1. PATIENTS AND METHODS The level of IL-6 mRNA in 48 paired NSCLC tissues and matched normal ones was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Kaplan-Meier curves were depicted for assessing the overall survival of NSCLC patients with high or low level of IL-6 mRNA. Subsequently, the ZEB2-AS1 level in A549 cells treated with different doses of IL-6 for different time points was determined. After A549 cells were treated with different doses of IL-6, wound closure assays were performed to assess the migration of cells. Protein levels of pSTAT1 and STAT1 in IL-6-treated A549 cells were detected by Western blot. The regulatory effect of STAT1 on IL-6-induced migration of A549 cells was also evaluated. The interaction between ZEB2-AS1 and STAT1 was explored through Chromatin Immunoprecipitation (ChIP) assay. Finally, the role of ZEB2-AS1/STAT1 axis in regulating NSCLC cells was investigated through rescue experiments.
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