Zhi-Qiang Li
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Research Interests
Zhi-Qiang Li has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Sheng-Hua Chu
Department of Neurosurgery, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 201999, P.R. China
4 shared publications - Dong-Fu Feng
Department of Neurosurgery, Shanghai 3rd People's Hospital, School of Medicine, Shanghai Jiao Tong University, 280 Mohe Road, Baoshan District, Shanghai 201900, China
3 shared publications - Yan-Bin Ma
Department of Neurosurgery, Shanghai 3rd People's Hospital, School of Medicine, Shanghai Jiao Tong University, 280 Mohe Road, Baoshan District, Shanghai 201900, China
3 shared publications - Hong Zhang
Department of Neurosurgery, NO.3 People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 280 Mo He Road, Bao Shan District, Shanghai, 201900, China
2 shared publications - Pu-Cha Jiang
Department of Neurosurgery, Zhongnan Hospital of Wuhan University, Wuhan 430071, China
2 shared publications - Zhi-An Zhu
Department of Neurosurgery, NO.3 People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 280 Mo He Road, Bao Shan District, Shanghai, 201900, China
2 shared publications
Latest Publications
- Open Access
- 20 March 2013
- Published by Springer Nature in Journal of Translational Medicine
- Vol. 11 (1) , 69
Predictive value of the SLC22A18 protein expression in glioblastoma patients receiving temozolomide therapy
Our previous study showed that SLC22A18 downregulation and promoter methylation were associated with the development and progression of glioma and the elevated expression of SLC22A18 was found to increase the sensitivity of glioma U251 cells to the anticancer drug 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). In this study, we investigated the predictive value of SLC22A18 promoter methylation and protein expression in glioblastoma multiforme (GBM) patients receiving temozolomide (TMZ) therapy.
- 20 March 2013
- Published by Springer Nature in Journal of Translational Medicine
- Vol. 11 (1) , 69
Open AccessPredictive value of the SLC22A18 protein expression in glioblastoma patients receiving temozolomide therapy
Our previous study showed that SLC22A18 downregulation and promoter methylation were associated with the development and progression of glioma and the elevated expression of SLC22A18 was found to increase the sensitivity of glioma U251 cells to the anticancer drug 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). In this study, we investigated the predictive value of SLC22A18 promoter methylation and protein expression in glioblastoma multiforme (GBM) patients receiving temozolomide (TMZ) therapy.
- Open Access
- 28 July 2012
- Published by Springer Nature in Journal of Translational Medicine
- Vol. 10 (1) , 149
Upregulation of SATB1 is associated with the development and progression of glioma
Special AT-rich sequence-binding protein-1 (SATB1) has been reported to be expressed in several human cancers and may have malignant potential. This study was aimed at investigating the expression and potential role of SATB1 in human glioma.
- 28 July 2012
- Published by Springer Nature in Journal of Translational Medicine
- Vol. 10 (1) , 149
Open AccessUpregulation of SATB1 is associated with the development and progression of glioma
Special AT-rich sequence-binding protein-1 (SATB1) has been reported to be expressed in several human cancers and may have malignant potential. This study was aimed at investigating the expression and potential role of SATB1 in human glioma.
- Open Access
- 21 September 2011
- Published by Springer Nature in Journal of Translational Medicine
- Vol. 9 (1) , 156
Promoter methylation and downregulation of SLC22A18 are associated with the development and progression of human glioma
Downregulation of the putative tumor suppressor gene SLC22A18 has been reported in a number of human cancers. The aim of this study was to investigate the relationship between SLC22A18 downregulation, promoter methylation and the development and progression of human glioma.
- 21 September 2011
- Published by Springer Nature in Journal of Translational Medicine
- Vol. 9 (1) , 156
Open AccessPromoter methylation and downregulation of SLC22A18 are associated with the development and progression of human glioma
Downregulation of the putative tumor suppressor gene SLC22A18 has been reported in a number of human cancers. The aim of this study was to investigate the relationship between SLC22A18 downregulation, promoter methylation and the development and progression of human glioma.
- 2 November 2008
- Published by Springer Nature in Molecular Biology Reports
- Vol. 36 (7) , 1967-1975
Stabilization of hepatocyte growth factor mRNA by hypoxia-inducible factor 1
Hypoxia regulates expression of hepatocyte growth factor (HGF) by increasing its transcription and by stabilizing its mRNA. Despite the pivotal role of hypoxia-inducible factor 1 (HIF-1) in transcriptional activation of hypoxia-responsive genes, it is not known whether HIF-1 mediates hypoxia-induced stabilization of HGF mRNA. We constructed adenoviral vectors expressing either the wild-type HIF-1α (Ad2/HIF-1α/FL), a constitutively stable hybrid form of HIF-1α (Ad2/HIF-1α/VP16), or no transgene (Ad2/CMVEV). In rat glioma (C6) cells, human glioma (U251) cells human cardiac, vascular smooth muscle, and endothelial cells, infection with Ad2/HIF-1α/VP16 or Ad2/HIF-1α/FL increased HGF expression at both the mRNA and protein levels. Under normoxic conditions, the half-life of HGF mRNA was 43 min in C6 and U251 cells. Hypoxia and Ad2/HIF-1α/VP16 increased the half-life of HGF mRNA to 3.2 and 2.8 h, respectively, while Ad2/CMVEV had no effect. These studies are the first to demonstrate that overexpression of HIF-1α increases HGF mRNA stability. Our results also suggest that stabilization of HGF mRNA by hypoxia is mediated, at least in part, by HIF-1.
- 2 November 2008
- Published by Springer Nature in Molecular Biology Reports
- Vol. 36 (7) , 1967-1975
Stabilization of hepatocyte growth factor mRNA by hypoxia-inducible factor 1
Hypoxia regulates expression of hepatocyte growth factor (HGF) by increasing its transcription and by stabilizing its mRNA. Despite the pivotal role of hypoxia-inducible factor 1 (HIF-1) in transcriptional activation of hypoxia-responsive genes, it is not known whether HIF-1 mediates hypoxia-induced stabilization of HGF mRNA. We constructed adenoviral vectors expressing either the wild-type HIF-1α (Ad2/HIF-1α/FL), a constitutively stable hybrid form of HIF-1α (Ad2/HIF-1α/VP16), or no transgene (Ad2/CMVEV). In rat glioma (C6) cells, human glioma (U251) cells human cardiac, vascular smooth muscle, and endothelial cells, infection with Ad2/HIF-1α/VP16 or Ad2/HIF-1α/FL increased HGF expression at both the mRNA and protein levels. Under normoxic conditions, the half-life of HGF mRNA was 43 min in C6 and U251 cells. Hypoxia and Ad2/HIF-1α/VP16 increased the half-life of HGF mRNA to 3.2 and 2.8 h, respectively, while Ad2/CMVEV had no effect. These studies are the first to demonstrate that overexpression of HIF-1α increases HGF mRNA stability. Our results also suggest that stabilization of HGF mRNA by hypoxia is mediated, at least in part, by HIF-1.