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- 검색키워드
- 저자 : Peipei Mao (검색결과 3 건)
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Mao, Ping,Joshi, Kaushal,Li, Jianfeng,Kim, Sung-Hak,Li, Peipei,Santana-Santos, Lucas,Luthra, Soumya,Chandran, Uma R.,Benos, Panayiotis V.,Smith, Luke,Wang, Maode,Hu, Bo,Cheng, Shi-Yuan,Sobol, Robert W National Academy of Sciences 2013 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.110 No.21
<P>Tumor heterogeneity of high-grade glioma (HGG) is recognized by four clinically relevant subtypes based on core gene signatures. However, molecular signaling in glioma stem cells (GSCs) in individual HGG subtypes is poorly characterized. Here we identified and characterized two mutually exclusive GSC subtypes with distinct dysregulated signaling pathways. Analysis of mRNA profiles distinguished proneural (PN) from mesenchymal (Mes) GSCs and revealed a pronounced correlation with the corresponding PN or Mes HGGs. Mes GSCs displayed more aggressive phenotypes in vitro and as intracranial xenografts in mice. Further, Mes GSCs were markedly resistant to radiation compared with PN GSCs. The glycolytic pathway, comprising aldehyde dehydrogenase (ALDH) family genes and in particular ALDH1A3, were enriched in Mes GSCs. Glycolytic activity and ALDH activity were significantly elevated in Mes GSCs but not in PN GSCs. Expression of ALDH1A3 was also increased in clinical HGG compared with low-grade glioma or normal brain tissue. Moreover, inhibition of ALDH1A3 attenuated the growth of Mes but not PN GSCs. Last, radiation treatment of PN GSCs up-regulated Mes-associated markers and down-regulated PN-associated markers, whereas inhibition of ALDH1A3 attenuated an irradiation-induced gain of Mes identity in PN GSCs. Taken together, our data suggest that two subtypes of GSCs, harboring distinct metabolic signaling pathways, represent intertumoral glioma heterogeneity and highlight previously unidentified roles of ALDH1A3-associated signaling that promotes aberrant proliferation of Mes HGGs and GSCs. Inhibition of ALDH1A3-mediated pathways therefore might provide a promising therapeutic approach for a subset of HGGs with the Mes signature.</P>
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Guosong Shen,Pingya He,Yingying Mao,Peipei Li,Frank Luh,Guohui Ding,Xi Yong Liu,Yun Yen 한국유방암학회 2017 Journal of breast cancer Vol.20 No.2
Purpose: Uridine-cytidine kinase (UCK) 2 is a rate-limiting enzyme involved in the salvage pathway of pyrimidine-nucleotide biosynthesis. Recent studies have shown that UCK2 is overexpressed in many types of cancer and may play a crucial role in activating antitumor prodrugs in human cancer cells. In the current study, we evaluated the potential prognostic value of UCK2 in breast cancer. Methods: We searched public databases to explore associations between UCK2 gene expression and clinical parameters in patients with breast cancer. Gene set enrichment analysis (GSEA) was performed to identify biological pathways associated with UCK2 gene expression levels. Survival analyses were performed using 10 independent large-scale breast cancer microarray datasets. Results: We found that UCK2 mRNA expression was elevated in breast cancer tissue compared with adjacent nontumorous tissue or breast tissue from healthy controls. High UCK2 levels were correlated with estrogen receptor negativity (p<0.001), advanced tumor grade (p<0.001), and poor tumor differentiation (p<0.001). GSEA revealed that UCK2-high breast cancers were enriched for gene sets associated with metastasis, progenitor-like phenotypes, and poor prognosis. Multivariable Cox proportional hazards regression analyses of microarray datasets verified that high UCK2 gene expression was associated with poor overall survival in a dose-response manner. The prognostic power of UCK2 was superior to that of TNM staging and comparable to that of multiple gene signatures. Conclusion: These findings suggest that UCK2 may be a promising prognostic biomarker for patients with breast cancer.
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Linheng Li,Jing Gan,Xu Qu,Wenqi Lu,Peipei Mao,Bin Ran 대한토목학회 2021 KSCE Journal of Civil Engineering Vol.25 No.5
Safety and efficiency have always been significant challenges to the development of road traffic. Detailed vehicle motion information is the prerequisite for achieving optimal control of the platoon and improving traffic safety and efficiency. The connected and automated vehicles (CAVs) system has offered unprecedented opportunities for the real-time collection and processing of these detailed vehicle motion data. Based on the model predictive control (MPC) framework and safety potential field (SPF) model, we developed an alternative CAVs platoon dynamic control method. The SPF model was applied to describe the road risk distribution under the complex driving environment and was embedded in the MPC framework to optimize the vehicle dynamics from the perspective of capacity, safety, and energy-saving. Also, some experiments were performed to verify the validity of our platoon control strategy. Compared with the fixed time-headway strategy, our proposed strategy can increase the traffic capacity by about 24.4%, while ensuring safety and improving fuel economy. The results indicate that the novel CAVs platoon control methodology proposed in this paper can be potentially applied to alleviate various traffic problems (e.g., traffic congestion, traffic accidents, and high emissions).
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