Warnerkoch7941

OBJECTIVE The importance of the circular ribonucleic acid (RNA) in malignant tumors causes more attention of researchers. Melanoma is one of the most ordinary malignant tumors. This study aims to identify how circ_0017247 functions in the progression of melanoma. PATIENTS AND METHODS Circ_0017247 expression of both melanoma patients' tissue samples and cell lines were detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the function of circ_0017247 was identified by performing the Wound healing assay, the transwell assay, and the Matrigel assay in vitro. Besides, the mechanism assays were performed to uncover the interaction between circ_0017247 and miR-145. In addition, the tumor metastasis assays were also conducted in vivo. RESULTS In this study, circ_0017247 expression was significantly higher in melanoma tissues compared with that in the skin tissues with a melanocytic nevus. The migrated length of the melanoma cells was reduced after circ_0017247 was silenced. Moreover, the number of migrated and invaded melanoma cells was reduced after circ_0017247 was silenced. Further experiments revealed that miR-145 was upregulated via knockdown of circ_0017247 and was also a direct target of circ_0017247 in melanoma. Furthermore, the tumor metastasis of melanoma was inhibited via knockdown of circ_0017247 in nude mice. CONCLUSIONS Our study suggests that circ_0017247 enhances melanoma cell migration and invasion via targeting miR-145 in vitro and in vivo.OBJECTIVE This study aimed to explore the effects of microRNA-29b (miR-29b) on chemoresistance of glioma and to examine the underlying mechanisms. MATERIALS AND METHODS MiR-29b expression in glioma tissues and cell lines was analyzed by quantitative real time-polymerase chain reaction (qRT-PCR). The cell viability was determined by Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was analyzed by Annexin V-Fluorescein isothiocyanate (FITC) assay. The relationship between miR-29b and signal transducer and activator of transcription 3 (STAT3) was examined by the Dual-Luciferase reporter gene assay. The levels of cleaved caspase-3, Bax, Bcl-2, and STAT3 were detected by Western blotting assay. RESULTS The expression of miR-29b was downregulated in glioma tissues compared to normal brain tissue. In addition, the expression level of miR-29b was lower in glioma tissues from patients at late stages (III and IV) compared with early stages (I and II). Besides, miR-29b expression was significantly lower in LN229, U87MGulated Bcl-2 protein. As expected, the effect of miR-29b upregulation on cell growth and apoptosis of TMZ-resistant glioma cells was reversed by STAT3 overexpression. The results from the Luciferase assay demonstrated miR-29b modulated STAT3 expression by directly bound with 3'-Untranslated Region (3'-UTR). CONCLUSIONS MiR-29b enhances the cell sensitivity to TMZ by inhibiting STAT3 in glioma. Our study might provide a novel target for treating TMZ-resistant glioma.OBJECTIVE The aim of this study was to investigate the role of long noncoding ribonucleic acids (lncRNAs) AK024094 in regulating the progression of breast cancer (BCa) and the potential mechanism. learn more Our findings might help to provide a theoretical basis for the targeted therapy of BCa. PATIENTS AND METHODS The relative expression level of lncRNA AK024094 in BCa and adjacent normal tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The prognostic potential of AK024094 in BCa was assessed by the Kaplan-Meier method. Meanwhile, AK024094 level in BCa cell lines was detected by qRT-PCR as well. The regulatory effects of AK024094 on the proliferative, migratory, and invasive abilities of MDA-MB-468 and MCF-7 cells were evaluated by functional assays. The Dual-Luciferase Reporter Gene Assay was applied to verify the binding between AK024094 and miRNA-181a. In addition, the rescue experiments were conducted to uncover the role of AK024094/miRNA-181a in the progression of BCa. RESULTS BCa cells by targeting miRNA-181a.OBJECTIVE Breast cancer (BC) is an intractable cancer with a rising incidence. Small nucleolar RNA host gene 15 (SNHG15) is a novel biomarker of multiple cancers. However, the molecular mechanism of SNHG15 during oncogenesis of BC is still poorly understood. MATERIALS AND METHODS Expression of SNHG15, microRNA (miR)-411-5p and vasodilator stimulated phosphoprotein (VASP) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was evaluated by colony formation and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell apoptosis was determined by flow cytometry and caspase-3 activity assay. Cell migration and invasion were examined by transwell assay. The interaction between miR-411-5p and SNHG15 or VASP was validated by dual-luciferase reporter assay. Protein expression of VASP, B cell lymphoma (Bcl-2), Bcl-2 associated X (Bax), vascular endothelial growth factor (VEGF), and matrix metalloproteinases (MMP-9, MMP-14) was measured by Western blot. Xenograft mice were established by subcutaneously injecting SKBR-3 cells transfected with sh-SNHG15 and sh-NC. RESULTS SNHG15 and VASP were over-expressed whereas miR-411-5p was low-expressed in BC tumors and cells compared with the normal counterparts. Next, SNHG15 knockdown attenuated cell proliferation, migration, invasion and stimulated cell apoptosis in BC. In addition, SNHG15 acted as a sponge while VASP acted as a target of miR-411-5p. Rescue experiment revealed that miR-411-5p inhibitor could alleviate SNHG15 silencing-induced inhibitive effects on cell proliferation, migration, invasion and promotive effects on cell apoptosis. Similarly, VASP attenuated the regulatory effects of SNHG15 silencing on BC cell progression. Furthermore, SNHG15 elimination hindered tumor growth in vivo. CONCLUSIONS SNHG15 contributes to BC cell progression by sponging miR-411-5p and enhancing VASP expression, providing essential biomarkers for BC therapy.OBJECTIVE Breast cancer (BC) is the second most frequent malignancy worldwide. Hsa_circ_0008039 exerts the carcinogenic factors in BC. However, the pathogenesis of hsa_circ_0008039 involved in BC is still unclear. PATIENTS AND METHODS The expression levels of hsa_circ_0008039, microRNA-515-5p (miR-515-5p) and chromobox homolog 4 (CBX4) in BC tissues and cells were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, migration and invasion were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) and transwell assays, severally. The binding relationship among hsa_circ_0008039, miR-515-5p and CBX4 was predicted by starBase, then verified by the dual-luciferase reporter assay and immunoprecipitation (RIP) assay. The interaction between hsa_circ_0008039 and miR-515-5p was confirmed by RNA pull-down assay. The protein level of CBX4 was detected by Western blot assay. The biological role of hsa_circ_0008039 was detected by xenograft tumor model in vivo. RESULTS Hsa_circ_0008039 was upregulated in BC tissues and cells, and expedited proliferation, migration and invasion of BC cells. MiR-515-5p was downregulated in BC tissues and cells and worked as a target of hsa_circ_0008039. CBX4 was highly expressed in BC tissues and cells, and contributed to proliferation, migration and invasion of BC cells. Hsa_circ_0008039 enhanced CBX4 expression by competitively binding to miR-515-5p, thereby promoting BC development. Hsa_circ_0008039 knockdown repressed BC tumor growth in vivo. CONCLUSIONS These findings implicated that hsa_circ_0008039 contributed to proliferation, migration and invasion in vitro and promoted tumor growth in vivo by miR-515-5p/CBX4 axis in BC, suggesting a potential therapeutic strategy for BC treatment.OBJECTIVE Several plasma-derived exosome RNAs have been identified as key regulators in cancer development. They have been considered as potential biomarkers for a non-invasive "liquid biopsy" to diagnose and assess the progression of cancer. This study aimed to identify human lung adenocarcinoma-specific exosome RNAs in peripheral blood, while assessing the feasibility and efficiency of this recently developed deep-sequencing technology for transcriptome profiling. PATIENTS AND METHODS Plasma-derived exosome RNAs were isolated from 13 lung adenocarcinoma patients, 3 patients with benign lung diseases, and 15 healthy volunteers. RNA-seq analysis of ribosomal RNA-depleted total RNA was performed. RNAs differentially expressed between lung adenocarcinoma and benign lung diseases or healthy volunteers were identified, followed by GO and KEGG pathway enrichment analyses for the identification of key exosome RNAs associated with lung adenocarcinomas. RESULTS Significant differentially expressed RNAs, such as UDP gs.OBJECTIVE To detect the expression of long non-coding ribonucleic acid (lncRNA) ASB16-AS1 in non-small cell lung cancer (NSCLC) tissues and cells, and to explore the effect of lncRNA ASB16-AS1 on the biological functions of NSCLC cells. PATIENTS AND METHODS The expression level of lncRNA ASB16-AS1 in NSCLC tissues and cells was detected via real-time fluorescence quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). The interference sequences of lncRNA ASB16-AS1 were designed and synthesized, and its transfection efficacy was detected by qRT-PCR. After knockdown of lncRNA ASB16-AS1, the proliferation, cell cycle, and apoptosis of NSCLC cells were detected via cell counting kit-8 (CCK-8) assay, colony formation assay, and flow cytometry, respectively. Moreover, the expression changes in the Wnt/β catenin signaling pathway were detected via Western blotting. RESULTS LncRNA ASB16-AS1 was upregulated in NSCLC tissues and cells compared with that in paracarcinoma tissues and 16HBE cells. The results of CCK-8 assay and colony formation assay revealed that the silence of lncRNA ASB16-AS1 attenuated the proliferative ability in NSCLC. The results of flow cytometry manifested that the silence of lncRNA ASB16-AS1 arrested the cell cycle in G0/1 phase, and accelerated the apoptosis rate. The key proteins in the Wnt/β-catenin signaling pathway were regulated by lncRNA ASB16-AS1 in NSCLC. CONCLUSIONS LncRNA ASB16-AS1 is upregulated in NSCLC tissues and cells, which promotes proliferation and inhibits apoptosis of NSCLC cells through the Wnt/β-catenin signaling pathway.OBJECTIVE Researchers have uncovered the importance of circular RNAs (circ) in malignant tumors. Circ LARP4 has been found to serve as a tumor suppressor gene in gastric cancer. However, the exact function of circ LARP4 in non-small-cell lung cancer (NSCLC) has not been fully elucidated. The aim of this study was to uncover the role of circ LARP4 in the tumorigenesis of NSCLC. PATIENTS AND METHODS Expression level of circ LARP4 in NSCLC tissues was detected through Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Subsequently, the association between expression and patients' prognosis was analyzed. Circ LARP4 lentivirus was constructed and transfected into NSCLC cells. The effect of circ LARP4 on NSCLC cell migration and invasion was detected by function assays. Furthermore, Western blot was performed to analyze the expression of predicted protein of circ LARP4. RESULTS Compared with adjacent tissues, circ LARP4 was lowly expressed in NSCLC tissues. Meanwhile, expression of circ LARP4 was associated with the prognosis of NSCLC patients.