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Linhui Liang - One of the best experts on this subject based on the ideXlab platform.
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microrna 127 5p targets the biliverdin reductase b nuclear factor κb pathway to suppress cell growth in hepatocellular carcinoma cells
Cancer Science, 2016Co-Authors: Lin Huan, Chunyang Bao, Di Chen, Junwei Lian, Jie Ding, Shenglin Huang, Linhui LiangAbstract:Nuclear factor‐κB (NF‐κB) activation is one of the major mediators of inflammation‐induced cancer cell growth and progression. In previous studies, we screened a series of microRNAs (miRNAs) that targeted the NF‐κB signaling pathway. In this study, we showed that miR‐127‐5p suppressed NF‐κB activity through inhibition of p65 nuclear translocation. In addition, miR‐127‐5p also inhibited the transcription of downstream targets of the NF‐κB signaling pathway. While exploring the mechanism of the inhibition of NF‐κB activity by miR‐127‐5p, we found that miR‐127‐5p decreased the phosphorylation of p65. MicroRNA‐127‐5p inhibited the growth and colony formation of hepatocellular carcinoma (HCC) cells and decreased biliverdin reductase B (BLVRB) expression by directly binding to its 3′‐UTR. RNA interference of BLVRB suppressed HCC cell growth, whereas the overexpression of BLVRB promoted HCC cell growth. Furthermore, BLVRB blockade inhibited the phosphorylation of p65 protein and the expression of downstream targets of the NF‐κB signaling pathway, mimicking the function of miR‐127‐5p. The restoration of BLVRB in HCC cells overexpressing miR‐127‐5p impaired the suppression of HCC growth by miR‐127‐5p. Moreover, miR‐127‐5p was downregulated in 58% of HCC samples. In summary, we found that miR‐127‐5p suppressed NF‐κB activity by directly targeting BLVRB in HCC cells, and this finding improves our understanding of the molecular mechanism of inflammation‐induced HCC growth and proliferation and the successful inhibition of NF‐κB activity by cancer treatment.
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MicroRNA‐127‐5p targets the biliverdin reductase B/nuclear factor‐κB pathway to suppress cell growth in hepatocellular carcinoma cells
Cancer science, 2016Co-Authors: Lin Huan, Chunyang Bao, Di Chen, Junwei Lian, Jie Ding, Shenglin Huang, Linhui LiangAbstract:Nuclear factor-κB (NF-κB) activation is one of the major mediators of inflammation-induced cancer cell growth and progression. In previous studies, we screened a series of microRNAs (miRNAs) that targeted the NF-κB signaling pathway. In this study, we showed that Mir-127-5p suppressed NF-κB activity through inhibition of p65 nuclear translocation. In addition, Mir-127-5p also inhibited the transcription of downstream targets of the NF-κB signaling pathway. While exploring the mechanism of the inhibition of NF-κB activity by Mir-127-5p, we found that Mir-127-5p decreased the phosphorylation of p65. MicroRNA-127-5p inhibited the growth and colony formation of hepatocellular carcinoma (HCC) cells and decreased biliverdin reductase B (BLVRB) expression by directly binding to its 3'-UTR. RNA interference of BLVRB suppressed HCC cell growth, whereas the overexpression of BLVRB promoted HCC cell growth. Furthermore, BLVRB blockade inhibited the phosphorylation of p65 protein and the expression of downstream targets of the NF-κB signaling pathway, mimicking the function of Mir-127-5p. The restoration of BLVRB in HCC cells overexpressing Mir-127-5p impaired the suppression of HCC growth by Mir-127-5p. Moreover, Mir-127-5p was downregulated in 58% of HCC samples. In summary, we found that Mir-127-5p suppressed NF-κB activity by directly targeting BLVRB in HCC cells, and this finding improves our understanding of the molecular mechanism of inflammation-induced HCC growth and proliferation and the successful inhibition of NF-κB activity by cancer treatment.
Lin Huan - One of the best experts on this subject based on the ideXlab platform.
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microrna 127 5p targets the biliverdin reductase b nuclear factor κb pathway to suppress cell growth in hepatocellular carcinoma cells
Cancer Science, 2016Co-Authors: Lin Huan, Chunyang Bao, Di Chen, Junwei Lian, Jie Ding, Shenglin Huang, Linhui LiangAbstract:Nuclear factor‐κB (NF‐κB) activation is one of the major mediators of inflammation‐induced cancer cell growth and progression. In previous studies, we screened a series of microRNAs (miRNAs) that targeted the NF‐κB signaling pathway. In this study, we showed that miR‐127‐5p suppressed NF‐κB activity through inhibition of p65 nuclear translocation. In addition, miR‐127‐5p also inhibited the transcription of downstream targets of the NF‐κB signaling pathway. While exploring the mechanism of the inhibition of NF‐κB activity by miR‐127‐5p, we found that miR‐127‐5p decreased the phosphorylation of p65. MicroRNA‐127‐5p inhibited the growth and colony formation of hepatocellular carcinoma (HCC) cells and decreased biliverdin reductase B (BLVRB) expression by directly binding to its 3′‐UTR. RNA interference of BLVRB suppressed HCC cell growth, whereas the overexpression of BLVRB promoted HCC cell growth. Furthermore, BLVRB blockade inhibited the phosphorylation of p65 protein and the expression of downstream targets of the NF‐κB signaling pathway, mimicking the function of miR‐127‐5p. The restoration of BLVRB in HCC cells overexpressing miR‐127‐5p impaired the suppression of HCC growth by miR‐127‐5p. Moreover, miR‐127‐5p was downregulated in 58% of HCC samples. In summary, we found that miR‐127‐5p suppressed NF‐κB activity by directly targeting BLVRB in HCC cells, and this finding improves our understanding of the molecular mechanism of inflammation‐induced HCC growth and proliferation and the successful inhibition of NF‐κB activity by cancer treatment.
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MicroRNA‐127‐5p targets the biliverdin reductase B/nuclear factor‐κB pathway to suppress cell growth in hepatocellular carcinoma cells
Cancer science, 2016Co-Authors: Lin Huan, Chunyang Bao, Di Chen, Junwei Lian, Jie Ding, Shenglin Huang, Linhui LiangAbstract:Nuclear factor-κB (NF-κB) activation is one of the major mediators of inflammation-induced cancer cell growth and progression. In previous studies, we screened a series of microRNAs (miRNAs) that targeted the NF-κB signaling pathway. In this study, we showed that Mir-127-5p suppressed NF-κB activity through inhibition of p65 nuclear translocation. In addition, Mir-127-5p also inhibited the transcription of downstream targets of the NF-κB signaling pathway. While exploring the mechanism of the inhibition of NF-κB activity by Mir-127-5p, we found that Mir-127-5p decreased the phosphorylation of p65. MicroRNA-127-5p inhibited the growth and colony formation of hepatocellular carcinoma (HCC) cells and decreased biliverdin reductase B (BLVRB) expression by directly binding to its 3'-UTR. RNA interference of BLVRB suppressed HCC cell growth, whereas the overexpression of BLVRB promoted HCC cell growth. Furthermore, BLVRB blockade inhibited the phosphorylation of p65 protein and the expression of downstream targets of the NF-κB signaling pathway, mimicking the function of Mir-127-5p. The restoration of BLVRB in HCC cells overexpressing Mir-127-5p impaired the suppression of HCC growth by Mir-127-5p. Moreover, Mir-127-5p was downregulated in 58% of HCC samples. In summary, we found that Mir-127-5p suppressed NF-κB activity by directly targeting BLVRB in HCC cells, and this finding improves our understanding of the molecular mechanism of inflammation-induced HCC growth and proliferation and the successful inhibition of NF-κB activity by cancer treatment.
Wei Liu - One of the best experts on this subject based on the ideXlab platform.
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Hsa_circ_0015326 Promotes the Proliferation, Invasion and Migration of Ovarian Cancer Through Mir-127-3p/MYB.
Cancer management and research, 2021Co-Authors: Cuiying Zhang, Wei Liu, Yang Feng, Jia WangAbstract:Background More and more evidences show that circular RNA (circRNA) has an important role in ovarian cancer (OC). Hsa_circ_0015326 is a newly discovered upregulated circRNA in OC, but its role and mechanism in OC have not been studied yet. Methods Quantitative real-time PCR was used to detect the expression of hsa_circ_0015326, microRNA (miR)-127-3p and MYB. The viability, colony number, cell cycle process, invasion, migration and apoptosis of cells were determined using cell counting kit 8 assay, colony formation assay, flow cytometry, transwell assay and wound healing assay. Moreover, the protein expression levels of metastasis, proliferation, apoptosis markers and MYB were assessed using Western blot analysis. The interaction between Mir-127-3p and hsa_circ_0015326 or MYB was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation assay. Xenograft tumors were built to explore the role of hsa_circ_0015326 in OC tumor growth in vivo. Results Elevated expression of hsa_circ_0015326 was identified in OC tissues and cells. Loss-of-function experiments suggested that silenced hsa_circ_0015326 inhibited the proliferation, invasion, migration, and promoted the apoptosis of OC cells in vitro, as well as inhibited OC tumorigenesis in vivo. Mechanically, hsa_circ_0015326 sponged Mir-127-3p and Mir-127-3p targeted MYB. The rescue experiments revealed that Mir-127-3p inhibitor reversed the inhibitory effect of hsa_circ_0015326 silencing on OC progression, and MYB overexpression reversed the suppressive effect of Mir-127-3p on OC progression. In addition, our data indicated that MYB expression was positively regulated by hsa_circ_0015326. Conclusion This study showed that hsa_circ_0015326 could facilitate OC progression by regulating the Mir-127-3p/MYB axis, which suggested that it might become a potential target for the treatment of OC.
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Dysregulated Mir-127-5p contributes to type II collagen degradation by targeting matrix metalloproteinase-13 in human intervertebral disc degeneration.
Biochimie, 2017Co-Authors: Wenbin Hua, Yukun Zhang, Yu Song, Liang Kang, Kangcheng Zhao, Kun Wang, Wei LiuAbstract:Abstract Background Intervertebral disc degeneration (IDD) is a chronic disease associated with the degradation of extracellular matrix (ECM). Matrix metalloproteinase (MMP)-13 is a major enzyme that mediates the degradation of ECM components. MMP-13 has been predicted to be a potential target of Mir-127-5p. However, the exact function of Mir-127-5p in IDD is still unclear. Objective We designed this study to evaluate the correlation between Mir-127-5p level and the degeneration of human intervertebral discs and explore the potential mechanisms. Methods Mir-127-5p levels and MMP-13 mRNA levels were detected by quantitative real-time polymerase chain reaction (qPCR). To determine whether MMP-13 is a target of Mir-127-5p, dual luciferase reporter assays were performed. Mir-127-5p mimic and Mir-127-5p inhibitor were used to overexpress or downregulate Mir-127-5p expression in human NP cells, respectively. Small interfering RNA (siRNA) was used to knock down MMP-13 expression in human NP cells. Type II collagen expression in human NP cells was detected by qPCR, western blotting, and immunofluorescence staining. Results We confirmed that Mir-127-5p was significantly downregulated in nucleus pulposus (NP) tissue of degenerative discs and its expression was inversely correlated with MMP-13 mRNA levels. We reveal that MMP-13 may act as a target of Mir-127-5p. Expression of Mir-127-5p was inversely correlated with type II collagen expression in human NP cells. Moreover, suppression of MMP-13 expression by siRNA blocked downstream signaling and increased type II collagen expression. Conclusion Dysregulated Mir-127-5p contributed to the degradation of type II collagen by targeting MMP-13 in human IDD. Our findings highlight that Mir-127-5p may serve as a new therapeutic target in IDD.
Hyun Ah Kim - One of the best experts on this subject based on the ideXlab platform.
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microrna 127 5p regulates matrix metalloproteinase 13 expression and interleukin 1β induced catabolic effects in human chondrocytes
Arthritis & Rheumatism, 2013Co-Authors: Su Jin Park, Eun Jeong Cheon, Mi Hyun Lee, Hyun Ah KimAbstract:Objective MicroRNAs (miRNAs), small noncoding RNA molecules, are involved in the pathogenesis of various diseases such as cancer and arthritis. The aim of this study was to determine whether Mir-127-5p regulates interleukin-1β (IL-1β)–induced expression of matrix metalloproteinase 13 (MMP-13) and other catabolic factors in human chondrocytes. Methods Expression of Mir-127-5p and MMP-13 by normal and osteoarthritic (OA) human cartilage was determined using real-time polymerase chain reaction. The effect of Mir-127-5p on MMP-13 expression was evaluated using transient transfection of human chondrocytes or chondrogenic SW-1353 cells with Mir-127-5p or its antisense inhibitor (anti–Mir-127-5p). MMP-13 protein production was quantified by enzyme-linked immunosorbent assay, and the involvement of Mir-127-5p in IL-1β–mediated catabolic effects was examined by immunoblotting. MicroRNA-127-5p binding with the putative site in the 3′-untranslated region (3′-UTR) of MMP-13 messenger RNA (mRNA) was validated by luciferase reporter assay. Results There was a significant reduction in Mir-127-5p expression in OA cartilage compared with normal cartilage. Up-regulation of MMP-13 expression by IL-1β was correlated with down-regulation of Mir-127-5p expression in human chondrocytes. MicroRNA-127-5p suppressed IL-1β–induced MMP-13 production as well as the activity of a reporter construct containing the 3′-UTR of human MMP-13 mRNA. In addition, mutation of the Mir-127-5p binding site in the 3′-UTR of MMP-13 mRNA abolished Mir-127-5p–mediated repression of reporter activity. Conversely, treatment with anti–Mir-127-5p remarkably increased reporter activity and MMP-13 production. Interestingly, the IL-1β–induced activation of JNK, p38, and NF-κB and expression of MMP-1 and cyclooxygenase 2 were significantly inhibited by Mir-127-5p. Conclusion MicroRNA-127-5p is an important regulator of MMP-13 in human chondrocytes and may contribute to the development of OA.
Jae-geun Yoon - One of the best experts on this subject based on the ideXlab platform.
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MicroRNA-127-3p promotes glioblastoma cell migration and invasion by targeting the tumor-suppressor gene SEPT7.
Oncology reports, 2014Co-Authors: Huawei Jiang, Dasong Hua, Jing Zhang, Qing Lan, Qiang Huang, Jae-geun Yoon, Xu Han, Gregory Foltz, Shu ZhengAbstract:MicroRNAs (miRNAs) are small non-coding RNAs of 20-25 nucleotides in length that are capable of modulating gene expression post-transcriptionally. The potential roles of miRNAs in the tumorigenesis of glioblastoma (GBM) have been under intensive studies in the past few years. In the present study, we found a positive correlation between the levels of Mir-127-3p and the cell migration and invasion abilities in several human GBM cell lines. We showed that Mir-127-3p promoted cell migration and invasion of GBM cells using in vitro cell lines and in vivo mouse models. We identified SEPT7, a known tumor-suppressor gene that has been reported to suppress GBM cell migration and invasion, as a direct target of Mir-127-3p. SEPT7 was able to partially abrogate the effect of Mir-127-3p on cell migration and invasion. In addition, microarray analysis revealed that Mir-127-3p regulated a number of migration and invasion-related genes. Finally, we verified that Mir-127-3p affected the remodeling of the actin cytoskeleton mediated by SEPT7 in GBM cells.
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Next generation sequencing analysis of miRNAs: Mir-127-3p inhibits glioblastoma proliferation and activates TGF-β signaling by targeting SKI.
Omics : a journal of integrative biology, 2014Co-Authors: Huawei Jiang, Dasong Hua, Qing Lan, Qiang Huang, Chengmeng Jin, Jie Liu, Fan Zhou, Xiaoyan Lou, Na Zhao, Jae-geun YoonAbstract:Glioblastoma (GBM) proliferation is a multistep process during which the expression levels of many genes that control cell proliferation, cell death, and genetic stability are altered. MicroRNAs (miRNAs) are emerging as important modulators of cellular signaling, including cell proliferation in cancer. In this study, using next generation sequencing analysis of miRNAs, we found that Mir-127-3p was downregulated in GBM tissues compared with normal brain tissues; we validated this result by RT-PCR. We further showed that DNA demethylation and histone deacetylase inhibition resulted in downregulation of Mir-127-3p. We demonstrated that Mir-127-3p overexpression inhibited GBM cell growth by inducing G1-phase arrest both in vitro and in vivo. We showed that Mir-127-3p targeted SKI (v-ski sarcoma viral oncogene homolog [avian]), RGMA (RGM domain family, member A), ZWINT (ZW10 interactor, kinetochore protein), SERPINB9 (serpin peptidase inhibitor, clade B [ovalbumin], member 9), and SFRP1 (secreted frizzled-related protein 1). Finally, we found that Mir-127-3p suppressed GBM cell growth by inhibiting tumor-promoting SKI and activating the tumor suppression effect of transforming growth factor-β (TGF-β) signaling. This study showed, for the first time, that Mir-127-3p and its targeted gene SKI, play important roles in GBM and may serve as potential targets for GBM therapy.