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Featured researches published by Shao Xie.


Biochemical and Biophysical Research Communications | 2013

GOLPH3 regulates the migration and invasion of glioma cells though RhoA

Xiuping Zhou; Wenjian Zhan; Wenbin Bian; Lei Hua; Qiong Shi; Shao Xie; Dongxu Yang; Yanwei Li; Xu Zhang; Guanzheng Liu; Rutong Yu

Golgi phosphoprotein 3 (GOLPH3) has been reported to be involved in the development of several human cancers. However, the biological significance of GOLPH3 in glioma progression remains largely unknown. In this study, we report, for the first time, that downregulation of GOLPH3 led to clear reductions in glioma cell migration and invasion. In addition, downregulation of GOLPH3 inhibited the expression of the small GTPase RhoA as well as cytoskeletal reorganization, which are both required for glioma cell migration. Furthermore, we found that the observed reductions in glioma cell migration and RhoA level could be rescued by RhoA overexpression. Taken together, these results show that GOLPH3 contributes to the motility of glioma cells by regulating the expression of RhoA.


Molecular Carcinogenesis | 2015

GOLPH3 promotes glioblastoma cell migration and invasion via the mTOR-YB1 pathway in vitro

Xu Zhang; Zhijun Ding; Jianbing Mo; Ben Sang; Qiong Shi; Jinxia Hu; Shao Xie; Wenjian Zhan; Dong Lu; Minglin Yang; Wenbin Bian; Xiuping Zhou; Rutong Yu

The identification of genes involved in carcinogenesis and tumor progression is of great interest, since these genes might be possible as candidates for new tumor targeted therapy strategies. Our previous study shows that Golgi phosphoprotein 3 (GOLPH3) is involved in glioma cell migration and invasion, the critical characteristics of malignant gliomas. In this study, we explored the mechanism of GOLPH3 affecting cell migration and invasion and found that GOLPH3 promotes glioblastoma (GBM) cell migration and invasion via the mammalian target of rapamycin(mTOR)‐Y‐box binding protein‐1 (YB1) pathway in vitro. Both the protein levels of GOLPH3 and YB1 were up‐regulated in human glioma tissues and they exhibited direct correlation with each other. In addition, down‐regulation of GOLPH3 inhibited glioma cell migration and invasion, while over‐expression of GOLPH3 enhanced them. Meanwhile, GOLPH3 down‐regulation led to a significant decrease of YB1 level as well as mTOR activity, both required for glioma cell migration and invasion. On the contrary, YB1 level and mTOR activity increased after GOLPH3 over‐expression. YB1 down‐regulation or mTOR ATP site inhibitor INK128 treatment inhibited cell migration and invasion, similar to the effect of GOLPH3 down‐regulation. Furthermore, over‐expression of GOLPH3 induced glioma cell migration and invasion was blocked by INK128 and YB1 down‐regulation. Taken together, these results show that GOLPH3 promotes glioblastoma cell migration and invasion via the mTOR‐YB1pathway, indicating that GOLPH3‐mTOR‐YB1 pathway might be a new therapeutic target for glioma treatment.


Cancer Letters | 2014

Protein kinase D2 promotes the proliferation of glioma cells by regulating Golgi phosphoprotein 3

Xiuping Zhou; Pengfei Xue; Minglin Yang; Hengliang Shi; Dong Lu; Zhaohao Wang; Qiong Shi; Jinxia Hu; Shao Xie; Wenjian Zhan; Rutong Yu

Protein kinase D2 (PKD2) has been demonstrated to promote tumorigenesis in many types of cancers. However, how PKD2 regulates cancer cell growth is largely unknown. In this study, we found that over-expression of PKD2 promoted glioma cell growth but down-regulation of PKD2 inhibited it. Further investigation indicated that PKD2 down-regulation decreased the protein level of Golgi phosphoprotein 3(GOLPH3) as well as p-AKT level. On the contrary, over-expression of PKD2 increased the protein level of GOLPH3 and p-AKT. In addition, GOLPH3 exhibited similar effect on glioma cell growth to that of PKD2. Importantly, GOLPH3 down-regulation partially abolished glioma cell proliferation induced by PKD2 over-expression, while over-expression of GOLPH3 also partially rescued the inhibition effect of PKD2 down-regulation on glioma cell growth. Interestingly, the level of PKD2 and GOLPH3 significantly increased and was positively correlated in a cohort of glioma patients, as well as in patients from TCGA database. Taken together, these results reveal that PKD2 promotes glioma cell proliferation by regulating GOLPH3 and then AKT activation. Our findings indicate that both PKD2 and GOLPH3 play important roles in the progression of human gliomas and PKD2-GOLPH3-AKT signaling pathway might be a potential glioma therapeutic target.


Biochemical and Biophysical Research Communications | 2015

β-Catenin is involved in Bex2 down-regulation induced glioma cell invasion/migration inhibition

Er Nie; Xu Zhang; Shao Xie; Qiong Shi; Jinxia Hu; Qingming Meng; Xiuping Zhou; Rutong Yu

Previously, we found that brain expressed X-linked gene 2 (Bex2) regulates the invasion/migration ability of glioma cells. However, the mechanism of this effect remains unknown. In current study, we reported that Bex2 down-regulation inhibited glioma cell migration and invasion by decreasing the nucleus and cytoplasm protein level of β-catenin. We found that the protein levels of Bex2 and β-catenin were up-regulated and showed direct correlation in glioma tissues. Bex2 down-regulation significantly decreased β-catenin protein levels but not its mRNA levels. Furthermore, the decreased protein level of β-catenin was located in the nucleus and cytoplasm but not in the cell membrane. Further study found that the effects of Bex2 down-regulation on the invasion and migration of glioma cell could be reversed by β-catenin over-expression. Taken together, Bex2 affects the invasion and migration ability of glioma cells by regulating β-catenin.


Cell Biology International | 2014

Over‐expression of Rap2a inhibits glioma migration and invasion by down‐regulating p‐AKT

Lei Wang; Wenjian Zhan; Shao Xie; Jinxia Hu; Qiong Shi; Xiuping Zhou; Yuxuan Wu; Shiquan Wang; Zhou Fei; Rutong Yu

Ras‐oncogenic pathway contributes to the pathogenesis of various tumours in humans, in which mutations of three canonical genes including H‐Ras, N‐Ras and K‐Ras are the most common events. Dysregulation of Ras signalling can be tumourigenic, especially gliomas of the central nervous system. Rap proteins are members of the small GTPase superfamily that involved in many biological processes. However, it remains largely unclear as to whether and how Rap proteins are involved in the development of multiple gliomas. We found that the levels of the protein Rap2a and the activity of Rap2a (GTP‐Rap2a) were weakly expressed in glioma tissues. Overexpressed Rap2a significantly inhibited the migration and invasion of glioma cells with an increase of GTP‐Rap2a. Overexpression of the dominant‐active (DA‐Rap2a), but not the dominant‐negative (DN‐Rap2a) form of Rap2a, also similarly inhibited the migration and invasion of glioma cells by reducing the phosphorylation level of AKT. In contrast, downregulation of Rap2a promoted glioma migration and invasion, and raised the phosphorylation level of AKT, whereas these effects were inhibited by PI3K‐specific inhibitor, LY294002. Thus unlike the other family members of Ras, Rab2a probably serves as a tumour suppressor in the pathogenesis of glioma.


Cell Biology International | 2015

Bmi‐1 regulates the migration and invasion of glioma cells through p16

Jun Liang; Peng Wang; Shao Xie; Weifeng Wang; Xiuping Zhou; Jinxia Hu; Qiong Shi; Xianli Zhang; Rutong Yu

Bmi‐1 is involved in the development of several human cancers; however, its significance in glioma progression remains largely unknown. We report that downregulation of Bmi‐1 clearly reduces glioma cell migration and invasion. Downregulation of Bmi‐1 promotes the expression of the tumor suppressor p16, which is important in glioma cell motility. Reduction in glioma cell invasion due to downregulation of Bmi‐1 could be rescued by p16 downregulation. These results show that Bmi‐1 contributes to the motility of glioma cells by regulating the expression of p16.


Neuro-oncology | 2017

Golgi phosphoprotein 3 promotes glioma progression via inhibiting Rab5-mediated endocytosis and degradation of epidermal growth factor receptor

Xiuping Zhou; Shao Xie; Shishuang Wu; Yanhua Qi; Zhaohao Wang; Hao Zhang; Dong Lu; Xu Wang; Yu Dong; Guanzheng Liu; Dongxu Yang; Qiong Shi; Wenbin Bian; Rutong Yu

Background Golgi phosphoprotein 3 (GOLPH3) is associated with worse prognosis of gliomas, but its role and mechanism in glioma progression remain largely unknown. This study aimed to explore the role and mechanism of GOLPH3 in glioma progression. Methods The expression of GOLPH3 in glioma tissues was detected by quantitative PCR, immunoblotting, and immunohistochemistry. GOLPH3s effect on glioma progression was examined using cell growth assays and an intracranial glioma model. The effect of GOLPH3 on epidermal growth factor receptor (EGFR) stability, endocytosis, and degradation was examined by immunoblotting and immunofluorescence. The activity of Rab5 was checked by glutathione S-transferase pulldown assay. Results GOLPH3 was upregulated in gliomas, and its downregulation inhibited glioma cell proliferation both in vitro and in vivo. Furthermore, GOLPH3 depletion dampened EGFR signaling by enhancing EGFR endocytosis, driving EGFR into late endosome and promoting lysosome-mediated degradation. Interestingly, GOLPH3 bound to Rab5 and GOLPH3 downregulation promoted the activation of Rab5. In addition, Rab5 depletion abolished the effect of GOLPH3 on EGFR endocytosis and degradation. Conclusion Our results imply that GOLPH3 promotes glioma cell proliferation via inhibiting Rab5-mediated endocytosis and degradation of EGFR, thereby activating the phosphatidylinositol-3 kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR) signaling pathway. We find a new mechanism by which GOLPH3 promotes tumor progression through regulating cell surface receptor trafficking. Extensive and intensive understanding of the role of GOLPH3 in glioma progression may provide an opportunity to develop a novel molecular therapeutic target for gliomas.


Oncology Letters | 2017

β‑transducin repeat‑containing E3 ubiquitin protein ligase inhibits migration, invasion and proliferation of glioma cells

Jun Liang; Wei‑Feng Wang; Shao Xie; Xian‑Li Zhang; Wei‑Feng Qi; Xiu‑Ping Zhou; Jin‑Xia Hu; Qiong Shi; Ru‑Tong Yu

β-transducin repeat-containing E3 ubiquitin protein ligase (β-TrCP) serves as the substrate recognition subunit for the Skp1-Cullin1-F-box protein E3 ubiquitin ligase, which recognizes the double phosphorylated DSG (X)2+nS destruction motif in various substrates that are essential for numerous aspects of tumorigenesis and regulates several important signaling pathways. However, the biological significance of β-TrCP in glioma progression remains largely unknown. A previous study by the authors demonstrated that the levels of β-TrCP protein expression in brain glioma tissues were significantly lower compared with non-tumorous tissues and that higher grades of gliomas exhibited lower levels of β-TrCP expression in comparison with lower glioma grades. In addition, low β-TrCP expression was associated with poor prognosis in patients with glioma. Subsequently, the present study aimed to investigate the effect of β-TrCP on migratory, invasive and proliferative abilities of glioma cells. β-TrCP plasmids were transfected into cultured U251 and U87 glioma cells, and changes in migration, invasion and proliferation were analyzed using wound healing, Transwell and EdU assays. It was identified that the overexpression of β-TrCP inhibited migration, invasion and proliferation in glioma cells. In summary, these results indicate that β-TrCP may serve a protective role against the progression of glioma by suppressing cell migration, invasion and proliferation. The potential mechanism of β-TrCP I glioma cells requires additional investigation.


Oncology Reports | 2017

Regulation of glioma migration and invasion via modification of Rap2a activity by the ubiquitin ligase Nedd4-1

Lei Wang; Bingxin Zhu; Shiquan Wang; Yuxuan Wu; Wenjian Zhan; Shao Xie; Hengliang Shi; Rutong Yu

Νeuronal precursor cell expressed and developmentally downregulated protein (Nedd4-1) is an E3 ubiquitin ligase with critical roles in the pathogenesis of cancer. Herein, we demonstrated that Nedd4-1 protein was upregulated in glioma tissues vs. that in non-cancerous tissues by western blotting and immunohistochemistry. Scratch migration and Transwell chamber assays indicated that downregulation of Nedd4-1 significantly reduced the migration and invasion of the glioma cell lines U251 and U87. Conversely, overexpression of Nedd4-1 obviously enhanced the migratory and invasive capacities in both cell lines. To investigate the role of Nedd4-1 and the intracellular pathways involved, we performed pull-down and co-immunoprecipitation assays, and recognized that Nedd4-1, TNIK and Rap2a formed a complex. Moreover, Nedd4-1 selectively ubiquitinated its specific substrates, the wild-type Rap2a (WT-Rap2a) and dominant-active Rap2a (DA-Rap2a) rather than the dominant-negative Rap2a (DN-Rap2a) in the U251 cells. Subsequently, we demonstrated that Rap2a was robustly ubiquitinated by Nedd4-1 along with the K63-linked, but not the K48-linked ubiquitin chain, which significantly inhibited GTP-Rap2a activity by GST-RalGDS pull-down assay. To further verify whether the ubiquitination of Rap2a by Nedd4-1 regulated the migration and invasion of glioma cells, Nedd4-1, HA-tagged ubiquitin and its mutants as well as WT-Rap2a were co-transfected in the U251 and U87 cell lines. The results confirmed that Nedd4-1 inhibited GTP-Rap2a activity, and promoted the migration and invasion of glioma cells. In brief, our findings demonstrated the important role of Nedd4-1 in regulating the migration and invasion of glioma cells via the Nedd4-1/Rap2a pathway, which may qualify Nedd4-1 as a viable therapeutic target for glioma.


Journal of Cancer Research and Therapeutics | 2017

Expression of WW domain-containing protein 2 is correlated with pathological grade and recurrence of glioma

Jun Liang; Weifeng Qi; Shao Xie; Weifeng Wang; Xianli Zhang; Xiuping Zhou; Qiong-Shi; Jinxia Hu; Rutong Yu

OBJECTIVE WW domain-containing protein 2 (WWP2) is an E3 ubiquitin ligase, which belongs to the NEDD4-like protein family. Recently, it is reported to play a key role in tumorigenesis and development of tumors such as prostate and lung cancer. However, there has been not related report on glioma until now. The aim of this study is to detect the expression of WWP2 and analyze its correlation to the pathological grade and tumor recurrence in patients with glioma. MATERIALS AND METHODS Western blot and immunohistochemistry were separately used to detect the expression of WWP2 protein in 31 brain glioma tissue samples and 80 brain glioma paraffin specimens. The method of Kaplan-Meier was used to analyze the correlation between the WWP2 expression and glioma recurrence. RESULTS The protein expression level of WWP2 in glioma tissue was significantly higher than that in nontumorous brain tissue (P < 0.05), and the protein expression level of WWP2 in high-grade glioma (Grade III-IV) was significantly higher than that in low-grade glioma (Grade I-II) (P < 0.05). Kaplan-Meier analysis indicated that the patients with high WWP2 expression had significantly shorter tumor recurrence time than the patients with low WWP2 expression (P < 0.05). CONCLUSION Our study suggests that WWP2 may play a role in the genesis and development of glioma; it may be a potential biomarker to predict pathological grade and tumor recurrence in patients with glioma.

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Qiong Shi

Xuzhou Medical College

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Rutong Yu

Xuzhou Medical College

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Jinxia Hu

Xuzhou Medical College

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Jun Liang

Xuzhou Medical College

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Dong Lu

Xuzhou Medical College

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Wenbin Bian

Xuzhou Medical College

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