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38 results on '"Shi, Zhumei"'

12. SREBP2 maintains glioblastoma stem cells through keeping the balance between cholesterol biosynthesis and uptake

Author

Gu, Danling, primary, Zhou, Fengqi, additional, You, Hao, additional, Gao, Jiancheng, additional, Kang, Tao, additional, Dixit, Deobrat, additional, Wu, Qiulian, additional, Yang, Kailin, additional, Ci, Shusheng, additional, Shan, Danyang, additional, Fan, Xiao, additional, Yuan, Wei, additional, Zhang, Qian, additional, Lu, Chenfei, additional, Li, Daqi, additional, Zhao, Ningwei, additional, Shi, Zhumei, additional, Gao, Wei, additional, Lin, Fan, additional, Man, Jianghong, additional, Wang, Qianghu, additional, Qian, Xu, additional, Mack, Stephen C, additional, Tao, Weiwei, additional, Agnihotri, Sameer, additional, Zhang, Nu, additional, You, Yongping, additional, Rich, Jeremy N, additional, Zhang, Junxia, additional, and Wang, Xiuxing, additional

Published
2023
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13. PGC1α Degradation Suppresses Mitochondrial Biogenesis to Confer Radiation Resistance in Glioma

Author

Zhao, Mengjie, primary, Li, Yanhui, additional, Lu, Chenfei, additional, Ding, Fangshu, additional, Xu, Miao, additional, Ge, Xin, additional, Li, Mengdie, additional, Wang, Zhen, additional, Yin, Jianxing, additional, Zhang, Junxia, additional, Wang, Xiefeng, additional, Ge, Zehe, additional, Xiao, Hong, additional, Xiao, Yong, additional, Liu, Hongyi, additional, Liu, Wentao, additional, Cao, Yuandong, additional, Wang, Qianghu, additional, You, Yongping, additional, Wang, Xiuxing, additional, Yang, Kun, additional, Shi, Zhumei, additional, and Qian, Xu, additional

Published
2023
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19. β2-Microglobulin Maintains Glioblastoma Stem Cells and Induces M2-like Polarization of Tumor-Associated Macrophages

Author

Li, Daqi, primary, Zhang, Qian, additional, Li, Lu, additional, Chen, Kexin, additional, Yang, Junlei, additional, Dixit, Deobrat, additional, Gimple, Ryan C., additional, Ci, Shusheng, additional, Lu, Chenfei, additional, Hu, Lang, additional, Gao, Jiancheng, additional, Shan, Danyang, additional, Li, Yangqing, additional, Zhang, Junxia, additional, Shi, Zhumei, additional, Gu, Danling, additional, Yuan, Wei, additional, Wu, Qiulian, additional, Yang, Kailin, additional, Zhao, Linjie, additional, Qiu, Zhixin, additional, Lv, Deguang, additional, Gao, Wei, additional, Yang, Hui, additional, Lin, Fan, additional, Wang, Qianghu, additional, Man, Jianghong, additional, Li, Chaojun, additional, Tao, Weiwei, additional, Agnihotri, Sameer, additional, Qian, Xu, additional, Shi, Yu, additional, You, Yongping, additional, Zhang, Nu, additional, Rich, Jeremy N., additional, and Wang, Xiuxing, additional

Published
2022
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28. Role and mechanism of miR-222 in arsenic-transformed cells for inducing tumor growth

Author

Wang, Min, primary, Ge, Xin, additional, Zheng, Jitai, additional, Li, Dongmei, additional, Liu, Xue, additional, Wang, Lin, additional, Jiang, Chengfei, additional, Shi, Zhumei, additional, Qin, Lianju, additional, Liu, Jiayin, additional, Yang, Hushan, additional, Liu, Ling-Zhi, additional, He, Jun, additional, Zhen, Linlin, additional, and Jiang, Bing-Hua, additional

Published
2016
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29. GSK-3β regulates tumor growth and angiogenesis in human glioma cells

Author

Zhao, Peng, primary, Li, Qi, additional, Shi, Zhumei, additional, Li, Charlie, additional, Wang, Lin, additional, Liu, Xue, additional, Jiang, Chengfei, additional, Qian, Xu, additional, You, Yongping, additional, Liu, Ning, additional, Liu, Ling-Zhi, additional, Ding, Lianshu, additional, and Jiang, Bing-Hua, additional

Published
2015
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31. Alteration in Mir-21/PTEN Expression Modulates Gefitinib Resistance in Non-Small Cell Lung Cancer

Author

Shen, Hua, primary, Zhu, Fang, additional, Liu, Jinyuan, additional, Xu, Tongpeng, additional, Pei, Dong, additional, Wang, Rong, additional, Qian, Yingying, additional, Li, Qi, additional, Wang, Lin, additional, Shi, Zhumei, additional, Zheng, Jitai, additional, Chen, Qiudan, additional, Jiang, Binghua, additional, and Shu, Yongqian, additional

Published
2014
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32. MiR-124 governs glioma growth and angiogenesis and enhances chemosensitivity by targeting R-Ras and N-Ras

Author

Shi, Zhumei, primary, Chen, Qiudan, additional, Li, Chongyong, additional, Wang, Lin, additional, Qian, Xu, additional, Jiang, Chengfei, additional, Liu, Xue, additional, Wang, Xiefeng, additional, Li, Hai, additional, Kang, Chunsheng, additional, Jiang, Tao, additional, Liu, Ling-Zhi, additional, You, Yongping, additional, Liu, Ning, additional, and Jiang, Bing-Hua, additional

Published
2014
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33. Thomas Jefferson University, Department of Pathology, Anatomy and Cell Biology, Oral Administration of Apigenin Inhibits Metastasis through AKT/P70S6K1/MMP-9 Pathway in Orthotopic Ovarian Tumor Model.

Author

He, Jun, Xu, Qing, Wang, Min, Li, Chongyong, Qian, Xu, Shi, Zhumei, Liu, Ling-Zhi, Jiang, Bing-Hua, He, Jun, Xu, Qing, Wang, Min, Li, Chongyong, Qian, Xu, Shi, Zhumei, Liu, Ling-Zhi, and Jiang, Bing-Hua

Abstract

Apigenin, a flavonoid commonly present in the daily diet, is known for its potential anti-tumor properties. However, the effect of apigenin via oral administration on tumor growth and metastasis remains unknown. In this study we developed an orthotopic ovarian tumor model in nude mice to test the effect of apigenin oral administration, and showed that apigenin inhibited the micrometastasis of cancer cells in the animal tumor model. To understand the mechanism of apigenin in inhibiting metastasis, we found that apigenin greatly inhibited MMP-9 expression and p-AKT and p-p70S6K1 levels in the tumor tissues compared to the control group. We further demonstrated that the downregulation of MMP-9 by apigenin was mediated by the AKT/p70S6K1 pathway. These findings help to address the question with common interests to the public of whether oral uptake of flavonoids is effective in preventing cancer. Our results demonstrate for the first time that oral uptake of apigenin can inhibit tumor metastasis through MMP-9 expression using the orthotopic ovarian tumor model.

Published
2012

36. Dual Role of CXCL8 in Maintaining the Mesenchymal State of Glioblastoma Stem Cells and M2-Like Tumor-Associated Macrophages.

Author

Yuan W, Zhang Q, Gu D, Lu C, Dixit D, Gimple RC, Gao Y, Gao J, Li D, Shan D, Hu L, Li L, Li Y, Ci S, You H, Yan L, Chen K, Zhao N, Xu C, Lan J, Liu D, Zhang J, Shi Z, Wu Q, Yang K, Zhao L, Qiu Z, Lv D, Gao W, Yang H, Lin F, Wang Q, Man J, Li C, Tao W, Agnihotri S, Qian X, Mack SC, Zhang N, You Y, Rich JN, Sun G, and Wang X

Subjects
Humans, Animals, Mice, Tumor-Associated Macrophages metabolism, Phosphatidylinositol 3-Kinases metabolism, Cell Line, Tumor, Neoplastic Stem Cells metabolism, Cell Proliferation, Tumor Microenvironment genetics, Glioblastoma pathology, Brain Neoplasms pathology
Abstract

Purpose: The dynamic interplay between glioblastoma stem cells (GSC) and tumor-associated macrophages (TAM) sculpts the tumor immune microenvironment (TIME) and promotes malignant progression of glioblastoma (GBM). However, the mechanisms underlying this interaction are still incompletely understood. Here, we investigate the role of CXCL8 in the maintenance of the mesenchymal state of GSC populations and reprogramming the TIME to an immunosuppressive state., Experimental Design: We performed an integrative multi-omics analyses of RNA sequencing, GBM mRNA expression datasets, immune signatures, and epigenetic profiling to define the specific genes expressed in the mesenchymal GSC subsets. We then used patient-derived GSCs and a xenograft murine model to investigate the mechanisms of tumor-intrinsic and extrinsic factor to maintain the mesenchymal state of GSCs and induce TAM polarization., Results: We identified that CXCL8 was preferentially expressed and secreted by mesenchymal GSCs and activated PI3K/AKT and NF-κB signaling to maintain GSC proliferation, survival, and self-renewal through a cell-intrinsic mechanism. CXCL8 induced signaling through a CXCR2-JAK2/STAT3 axis in TAMs, which supported an M2-like TAM phenotype through a paracrine, cell-extrinsic pathway. Genetic- and small molecule-based inhibition of these dual complementary signaling cascades in GSCs and TAMs suppressed GBM tumor growth and prolonged survival of orthotopic xenograft-bearing mice., Conclusions: CXCL8 plays critical roles in maintaining the mesenchymal state of GSCs and M2-like TAM polarization in GBM, highlighting an interplay between cell-autonomous and cell-extrinsic mechanisms. Targeting CXCL8 and its downstream effectors may effectively improve GBM treatment., (©2023 American Association for Cancer Research.)

Published
2023
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37. Association between survivin -31G > C promoter polymorphism and cancer risk: a meta-analysis.

Author

Wang X, Huang L, Xu Y, Shi Z, Wang Y, Zhang J, Wang X, Cao L, Luo H, Chen J, Liu N, Yin Y, and You Y

Subjects
Alleles, Asian People genetics, Case-Control Studies, Confidence Intervals, Ethnicity genetics, Gene Frequency, Genetic Heterogeneity, Genotype, Humans, Neoplasms ethnology, Odds Ratio, Risk Factors, Sensitivity and Specificity, Survivin, Inhibitor of Apoptosis Proteins genetics, Neoplasms genetics, Polymorphism, Genetic, Promoter Regions, Genetic
Abstract

Survivin is an inhibitor of apoptosis protein and has a crucial role in the development of cancer. The survivin -31G>C (rs9904341) promoter polymorphism influences survivin expression and has been implicated in cancer risk. However, conflicting results have been published from studies on the association between survivin -31G>C polymorphism and the risk of cancer. To clarify the role of this polymorphism in cancer, we performed a meta-analysis of all available and relevant published studies, involving a total of 3485 cancer patients and 3964 control subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of the associations. The overall results indicated that the variant genotypes were associated with a significantly increased cancer risk (CC vs GG: OR=1.58, 95% CI=1.20-2.10; CC/GC vs GG: OR=1.23, 95% CI=1.00-1.51; CC vs GG/GC: OR=1.51, 95% CI=1.23-1.85). In the stratified analyses, significantly increased risk was associated with the Asian populations (CC vs GG: OR=1.67, 95% CI=1.16-2.40; CC vs GG/GC: OR=1.50, 95% CI=1.17-1.91). We also performed the analyses by cancer type, and no statistical association was observed. The results suggest that the survivin -31G>C promoter polymorphism might be associated with an increased risk of cancer, especially in the Asian populations.

Published
2012
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38. Updated meta-analysis of NFkappaB1 -94ins/Delattg promoter polymorphism and cancer risk based on 19 case-control studies.

Author

Wang X, Lu P, Xu L, Xu Y, Shi Z, Xu J, Wang Y, Zhang J, Wang X, Cao L, Liu N, Yin Y, and You Y

Subjects
Case-Control Studies, Gene Frequency, Genotype, Humans, INDEL Mutation, Polymorphism, Single Nucleotide, Risk Factors, Genetic Predisposition to Disease, NF-kappa B genetics, Neoplasms genetics, Promoter Regions, Genetic genetics
Abstract

Objective: Recently, a common insertion/deletion (-94insertion/deletion ATTG, rs28362491) polymorphism in the NFkappaB1 promoter region has been extensively investigated for association with cancer risk but the results have been inconsistent. In order to clarify the effect of the promoter polymorphism we performed an update meta-analysis of published case-control studies to better compare the results between studies., Methods: Relevant studies were identified via a thorough literature search on Medline and Embase database (up to August 10, 2011). The odds ratio (OR) and 95% confidence interval (95%CI) were used to investigate the strength of the association., Results: A total of 5,196 cases and 6,614 controls in 19 case-control studies from 16 publications were included in this meta-analysis. Overall, the variant genotypes were associated with a moderately decreased risk of all cancer types (OR =0.74, 95%CI =0.57-0.97 for DD versus II; OR =0.79, 95%CI =0.66-0.95 for DD versus II/ID). In the stratified analyses, significantly decreased risk was found among Asians (OR =0.52, 95%CI =0.42-0.65 for DD versus II; OR =0.74, 95%CI =0.66-0.83 for ID versus II; OR =0.64, 95%CI =0.53-0.78 for DD versus II/ID; OR =0.68, 95%CI =0.61-0.75 for DD/ID versus II). The validity of this association was further strengthened by the sensitivity analysis. No publication bias was observed in this study., Conclusions: Our results suggested that the -94deletion ATTG promoter polymorphism in NFkappaB1 gene might be associated with a decreased cancer risk, especially for Asian population.

Published
2011

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