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        miR-101 Inhibiting Cell Proliferation, Migration and Invasion in Hepatocellular Carcinoma through Downregulating Girdin

        Peiguo Cao,Ke Cao,Jingjing Li,Yong Zhao,Qi Wang,Qinghai Zeng,Siqi He,Li Yu,Jianda Zhou 한국분자세포생물학회 2016 Molecules and cells Vol.39 No.2

        miR-101 is considered to play an important role in hepatocellular carcinoma (HCC), but the underlying molecular mechanism remains to be elucidated. Here, we aimed to confirm whether Girdin is a target gene of miR-101 and determine the tumor suppressor of miR-101 through Girdin pathway. In our previous studies, we firstly found Girdin protein was overexpressed in HCC tissues, and it closely correlated to tumor size, T stage, TNM stage and Edmondson-Steiner stage of HCC patients. After specific small interfering RNA of Girdin was transfected into HepG2 and Huh7.5.1 cells, the proliferation and invasion ability of tumor cells were significantly inhibited. In this study, we further explored the detailed molecular mechanism of Girdin in HCC. Interestingly, we found that miR-101 significantly low-expressed in HCC tissues compared with that in matched normal tissues while Girdin had a relative higher expression, and miR-101 was inversely correlated with Girdin expression. In addition, after miR-101 transfection, the proliferation, migration and invasion abilities of HepG2 cells were weakened. Furthermore, we confirmed that Girdin is a direct target gene of miR-101. Finally we confirmed Talen-mediated Girdin knockout markedly suppressed cell proliferation, migration and invasion in HCC while down-regulation of miR-101 significantly restored the inhibitory effect. Our findings suggested that miR-101/Girdin axis could be a potential application of HCC treatment.

      • KCI등재

        Spectrum Cartography Based on Dynamic Compressed Sensing by Using Multiple Domains Information

        Xia, Haiyang,Huang, Jijun,Liu, Jibin,Liu, Peiguo,Zha, Song 한국통신학회 2023 Journal of communications and networks Vol.25 No.4

        Radio maps have experienced their success in ap-plications of wireless communications for years by offeringmetrics of radio frequency (RF) information, e.g., power spectraldensity (PSD), within a geographical region of interest. Spectrumcartography technique constructs radio maps to expand theabilities of RF awareness. However, seldom of existing methodsaim at constructing radio maps by utilizing multiple domains in-formation. In this paper, a novel framework inspired by dynamiccompressed sensing (DCS) has been proposed firstly to solve thisproblem. This flexible framework first to apply joint group-Lassofor PSD map construction based on the different sparse patternsbetween space and frequency domains as well as innovativelyutilizes transmitters’ mobility patterns for support prediction ofDCS. Simulation experiments have been processed to assess theperformance of methods within the proposed framework andframework’s superiority has been proven.

      • KCI등재

        miR-101 Inhibiting Cell Proliferation, Migration and Invasion in Hepatocellular Carcinoma through Downregulating Girdin

        Cao, Ke,Li, Jingjing,Zhao, Yong,Wang, Qi,Zeng, Qinghai,He, Siqi,Yu, Li,Zhou, Jianda,Cao, Peiguo Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.2

        miR-101 is considered to play an important role in hepatocellular carcinoma (HCC), but the underlying molecular mechanism remains to be elucidated. Here, we aimed to confirm whether Girdin is a target gene of miR-101 and determine the tumor suppressor of miR-101 through Girdin pathway. In our previous studies, we firstly found Girdin protein was overexpressed in HCC tissues, and it closely correlated to tumor size, T stage, TNM stage and Edmondson-Steiner stage of HCC patients. After specific small interfering RNA of Girdin was transfected into HepG2 and Huh7.5.1 cells, the proliferation and invasion ability of tumor cells were significantly inhibited. In this study, we further explored the detailed molecular mechanism of Girdin in HCC. Interestingly, we found that miR-101 significantly low-expressed in HCC tissues compared with that in matched normal tissues while Girdin had a relative higher expression, and miR-101 was inversely correlated with Girdin expression. In addition, after miR-101 transfection, the proliferation, migration and invasion abilities of HepG2 cells were weakened. Furthermore, we confirmed that Girdin is a direct target gene of miR-101. Finally we confirmed Talen-mediated Girdin knockout markedly suppressed cell proliferation, migration and invasion in HCC while downregulation of miR-101 significantly restored the inhibitory effect. Our findings suggested that miR-101/Girdin axis could be a potential application of HCC treatment.

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