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616 results on '"Song Libing"'

201. Hepatocellular carcinoma redirects to ketolysis for progression under nutrition deprivation stress

Author

Huang, De, primary, Li, Tingting, additional, Wang, Lin, additional, Zhang, Long, additional, Yan, Ronghui, additional, Li, Kui, additional, Xing, Songge, additional, Wu, Gongwei, additional, Hu, Lan, additional, Jia, Weidong, additional, Lin, Sheng-Cai, additional, Dang, Chi V, additional, Song, Libing, additional, Gao, Ping, additional, and Zhang, Huafeng, additional

Published
2016
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202. Serine-arginine protein kinase 1 promotes a cancer stem cell-like phenotype through activation of Wnt/β-catenin signalling in NSCLC

Author

Gong, Liyun, primary, Song, Junwei, additional, Lin, Xi, additional, Wei, Fakai, additional, Zhang, Cuicui, additional, Wang, Zimei, additional, Zhu, Jinrong, additional, Wu, Shu, additional, Chen, Yu, additional, Liang, Jin, additional, Fu, XiaoYuan, additional, Lu, Junqiang, additional, Zhou, Chunhui, additional, and Song, Libing, additional

Published
2016
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211. Targeting TRIM3deletion-induced tumor-associated lymphangiogenesis prohibits lymphatic metastasis in esophageal squamous cell carcinoma

Author

Zhu, Jinrong, Wu, Geyan, Ke, Zunfu, Cao, Lixue, Tang, Miaoling, Li, Ziwen, Li, Qiaojia, Zhou, Junhao, Tan, Zhanyao, Song, Libing, and Li, Jun

Abstract

Tumor-associated lymphangiogenesis has attracted increasing attention because of its potential contribution to lymph node metastasis. However, the molecular mechanisms underlying lymphangiogenesis in cancer remains elusive. In the current study, we demonstrate that tripartite motif-containing 3 (TRIM3) directly interacts with and induces E3 ligase-dependent proteasomal turnover of importin α3 and α-Actinin-4 (ACTN4), which controls nuclear factor kappa B (NF-κB) activity at a well-ordered level. Heterozygous deletion-mediated TRIM3 downregulation led to NF-κB constitutive activation through disruption of the NF-κB-IκB-α negative feedback loop and enhancement of the p65 DNA-binding affinity and transcriptional activity via promoting symmetrical dimethylarginine modification of NF-κB/p65 at Arg30 and Arg35, which consequently promoted lymphatic metastasis of esophageal squamous cell carcinoma (ESCC) cells. Treatment with Tecfidera, a medication used to treat multiple sclerosis, restored the negative feedback inhibition of NF-κB by reducing the NF-κB/ACTN4 interaction and decreasing symmetrically dimethylated NF-κB levels, resulting in inhibition of ESCC lymphatic metastasis both in vitro and in vivo. Taken together, our results uncover a novel mechanism for constitutive NF-κB activation in cancer and may represent an attractive strategy to treat ESCC lymphatic metastasis.

Published
2019
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212. Wnt5a induces and maintains prostate cancer cells dormancy in bone

Author

Ren, Dong, Dai, Yuhu, Yang, Qing, Zhang, Xin, Guo, Wei, Ye, Liping, Huang, Shuai, Chen, Xu, Lai, Yingrong, Du, Hong, Lin, Chuyong, Peng, Xinsheng, and Song, Libing

Abstract

In a substantial fraction of prostate cancer (PCa) patients, bone metastasis appears after years or even decades of latency. Canonical Wnt/β-catenin signaling has been proposed to be implicated in dormancy of cancer cells. However, how these tumor cells are kept dormant and recur under control of Wnt/β-catenin signaling derived from bone microenvironment remains unknown. Here, we report that Wnt5a from osteoblastic niche induces dormancy of PCa cells in a reversible manner in vitro and in vivo via inducing Siah E3 Ubiquitin Protein Ligase 2 (SIAH2) expression, which represses Wnt/β-catenin signaling. Furthermore, this effect of Wnt5a-induced dormancy of PCa cells depends on receptor tyrosine kinase-like orphan receptor 2 (ROR2), and a negative correlation of ROR2 expression with bone metastasis–free survival is observed in PCa patients. Therefore, these results demonstrate that Wnt5a/ROR2/SIAH2 signaling axis plays a crucial role in inducing and maintaining PCa cells dormancy in bone, suggesting a potential therapeutic utility of Wnt5a via inducing dormancy of PCa cells in bone.

Published
2019
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213. Integrated design on digital channelized reconnaissance and jamming

Author

Guo Bo, Chen Xinnian, and Song Libing

Subjects
Engineering, Pulse-Doppler radar, business.industry, Interlacing, Jamming, Fractional Fourier transform, law.invention, Condensed Matter::Soft Condensed Matter, law, Pulse compression, Frequency domain, Electronic engineering, Digital radio frequency memory, Radar, business
Abstract

With various interlacing signals, the electromagnetic environment of current battlefield becomes more and more dense and complex. It becomes more and more difficult to jam coherent radar especially with the ability of pulse compression. To achieve accurate and effective reconnaissance and jamming against coherent pulse compression radar, a method of integrated design based on digital channelized reconnaissance and jamming is proposed. In the system, the techniques of frequency domain sub-band processing, fractional fourier transform and convolution jamming are used in the design to increase its radar signal detection and denoising capabilities, while the jamming signals generated by a quickly matching method, which are coherent as much as possible, can realize effective jamming.

Published
2011

216. cMyc-mediated activation of serine biosynthesis pathway is critical for cancer progression under nutrient deprivation conditions

Author

Sun, Linchong, primary, Song, Libing, additional, Wan, Qianfen, additional, Wu, Gongwei, additional, Li, Xinghua, additional, Wang, Yinghui, additional, Wang, Jin, additional, Liu, Zhaoji, additional, Zhong, Xiuying, additional, He, Xiaoping, additional, Shen, Shengqi, additional, Pan, Xin, additional, Li, Ailing, additional, Wang, Yulan, additional, Gao, Ping, additional, Tang, Huiru, additional, and Zhang, Huafeng, additional

Published
2015
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218. CUE domain-containing protein 2 promotes the Warburg effect and tumorigenesis.

Author

Zhong, Xiuying, Tian, Shengya, Zhang, Xiang, Diao, Xinwei, Dong, Fangting, Yang, Jie, Li, Zhaoyong, Sun, Linchong, Wang, Lin, He, Xiaoping, Wu, Gongwei, Hu, Xin, Wang, Lihua, Song, Libing, Zhang, Huafeng, Pan, Xin, Li, Ailing, and Gao, Ping

Abstract

Cancer progression depends on cellular metabolic reprogramming as both direct and indirect consequence of oncogenic lesions; however, the underlying mechanisms are still poorly understood. Here, we report that CUEDC2 ( CUE domain-containing protein 2) plays a vital role in facilitating aerobic glycolysis, or Warburg effect, in cancer cells. Mechanistically, we show that CUEDC2 upregulates the two key glycolytic proteins GLUT3 and LDHA via interacting with the glucocorticoid receptor ( GR) or 14-3-3ζ, respectively. We further demonstrate that enhanced aerobic glycolysis is essential for the role of CUEDC2 to drive cancer progression. Moreover, using tissue microarray analysis, we show a correlation between the aberrant expression of CUEDC2, and GLUT3 and LDHA in clinical HCC samples, further demonstrating a link between CUEDC2 and the Warburg effect during cancer development. Taken together, our findings reveal a previously unappreciated function of CUEDC2 in cancer cell metabolism and tumorigenesis, illustrating how close oncogenic lesions are intertwined with metabolic alterations promoting cancer progression. [ABSTRACT FROM AUTHOR]

Published
2017
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228. TRIM14 promotes chemoresistance in gliomas by activating Wnt/β-catenin signaling via stabilizing Dvl2

Author

Tan, Zhanyao, Song, Libing, Wu, Wenjiao, Zhou, Yanqing, Zhu, Jinrong, Wu, Geyan, Cao, Lixue, Song, Junwei, Li, Jun, and Zhang, Wei

Abstract

Gliomas are a lethal class of brain cancer, with a median survival below 15 months in spite of therapeutic advances. The poor prognosis of this disease is largely attributed to acquired chemotherapy resistance, and new strategies are urgently needed to target resistant glioma cells. Herein, our study demonstrated that tripartite motif-containing 14 (TRIM14) overexpressed in glioma specimens (including tissues and cell lines), and that high level of TRIM14 predicted poor outcome of glioma patients. Furthermore, we found that upregulation of TRIM14 in glioma cells conferred chemoresistance to temozolomide in vitro and in vivo; conversely, silencing TRIM14 sensitized glioma cells to temozolomide. These findings demonstrated that TRIM14 stabilized dishevelled (Dvl2) and subsequently activated the canonical Wnt signaling and promoted chemoresistance. Moreover, inhibition of Dvl2 reversed the oncogenic effect of TRIM14 on chemoresistance. Importantly, consistent with the abovementioned results, we found that TRIM14 expression was significantly associated with hyperactivation of canonical Wnt pathway in clinical glioma specimens. Collectively, the study reveals a new molecular mechanism driving chemotherapy resistance in gliomas, and suggests an opportunity to develop novel therapeutic interventions against gliomas.

Published
2018
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229. A Wnt-induced lncRNA-DGCR5 splicing switch drives tumor-promoting inflammation in esophageal squamous cell carcinoma

Author

Li, Yue, Chen, Boyu, Jiang, Xingyu, Li, Yudong, Wang, Xin, Huang, Shumei, Wu, Xuxia, Xiao, Yunyun, Shi, Dongni, Huang, Xinjian, He, Lixin, Chen, Xiangfu, Ouyang, Ying, Li, Jun, Song, Libing, and Lin, Chuyong

Abstract

Alternative splicing (AS) is a critical mechanism for the aberrant biogenesis of long non-coding RNA (lncRNA). Although the role of Wnt signaling in AS has been implicated, it remains unclear how it mediates lncRNA splicing during cancer progression. Herein, we identify that Wnt3a induces a splicing switch of lncRNA-DGCR5 to generate a short variant (DGCR5-S) that correlates with poor prognosis in esophageal squamous cell carcinoma (ESCC). Upon Wnt3a stimulation, active nuclear β-catenin acts as a co-factor of FUS to facilitate the spliceosome assembly and the generation of DGCR5-S. DGCR5-S inhibits TTP’s anti-inflammatory activity by protecting it from PP2A-mediated dephosphorylation, thus fostering tumor-promoting inflammation. Importantly, synthetic splice-switching oligonucleotides (SSOs) disrupt the splicing switch of DGCR5 and potently suppress ESCC tumor growth. These findings uncover the mechanism for Wnt signaling in lncRNA splicing and suggest that the DGCR5 splicing switch may be a targetable vulnerability in ESCC.

Published
2023
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