Palmsantos1828

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. 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. ABBV-2222 modulator 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.