Activation of JAK/STAT signal pathway predicts poor prognosis of patients with gliomas

Tu, Yanyang; Zhong, Yi; Fu, Jianfang; Cao, Yangsen; Fu, Guangmiao; Tian, Xiaoxi; Wang, Boliang

doi:10.1007/s12032-010-9435-1

Cited by 69 publications

(48 citation statements)

References 29 publications

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“…As is known, hyper-activation of JAK1-STAT3 signaling pathway has close relationship to the development of certain types of human tumors. Previous studies reported that gliomas patients who possessed high-activation of JAK1 and STAT3 had lower overall survival rates than those with low JAK1 and STAT3 activation (23,27). When the JAK1-STAT3 pathway is activated, STAT3 will be phosphorylated and phosphorylated-STAT3 (p-STAT3) forms dimers and translocates into the nucleus to regulate expression of genes by binding to elements of their promoters.…”

Section: Discussionmentioning

confidence: 93%

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CUEDC2 suppresses glioma tumorigenicity by inhibiting the activation of STAT3 and NF-κB signaling pathway

Tang

Jin

et al. 2017

International Journal of Oncology

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CUEDC2, a CUE domain containing 2 protein, plays critical roles in many biological processes, such as cell cycle, inflammation and tumorigenesis. However, whether CUEDC2 was involved in tumorigenesis of glioma and the possible mechanism remains to be elucidated. In the present study, our results implied that the expression of CUEDC2 was lower in the glioma tissue and glioma cell lines than that of normal tissue and asctrocyte cells. Downregulation of endogenous CUEDC2 in glioma U251 cell lines by RNAi promoted the tumor cells proliferation, migration, invasion and glioma neurosphere formation, while, overexpression of CUEDC2 showed the opposite effect. Further studies showed that overexpression of CUEDC2 suppressed the activation and nuclear translocation of phosphorylated-STAT3 (p-STAT3) but the level of p-STAT3 increased after interfering with the expression of CUEDC2. Moreover, CUEDC2 expression has an inhibitory effect on the activation of NF-κB. Thus, our studies suggested that the decreased expression of CUEDC2 in glioma led to the activation of transcription factor STAT3 and NF-κB signaling pathway which may be related to the tumorigenicity in glioma.

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Section: Discussionmentioning

confidence: 93%

“…Activation of this pathway predicts poor prognosis of patients with gliomas (23). Therefore, whether CUEDC2 expression affects the JAK1-STAT3 pathway in transgenic U251 cells was investigated.…”

Section: Resultsmentioning

confidence: 99%

CUEDC2 suppresses glioma tumorigenicity by inhibiting the activation of STAT3 and NF-κB signaling pathway

Tang

Jin

et al. 2017

International Journal of Oncology

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“…An ontological analysis of the microarray data revealed 163 genes to be involved in cell cycle regulation, whose expression was modulated by WWOX overexpression. Among these genes are potent oncogenes linked with brain cancerogenesis: AURKA , KLF8 and JAK1 (12–16). In our microarray experiment, the T98G/ WWOX cells demonstrated significantly lower expression of all afore-mentioned genes.…”

Section: Discussionmentioning

confidence: 99%

WWOX modulates the gene expression profile in the T98G glioblastoma cell line rendering its phenotype less malignant

Kośla¹,

Nowakowska²,

Pospiech³

2014

Oncology Reports

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The aim of the present study was to assess the influence of WWOX gene upregulation on the transcriptome and phenotype of the T98G glioblastoma cell line. The cells with high WWOX expression demonstrated a significantly different transcription profile for approximately 3,000 genes. The main cellular pathways affected were Wnt, TGFβ, Notch and Hedgehog. Moreover, the WWOX-transfected cells proliferated at less than half the rate, exhibited greatly lowered adhesion to ECM, increased apoptosis and impaired 3D culture formation. They also demonstrated an increased ability for crossing the basement membrane. Our results indicate that WWOX, apart from its tumor-suppressor function, appears to be a key regulator of the main cellular functions of the cell cycle and apoptosis. Furthermore, our results showed that WWOX may be involved in controlling metabolism, cytoskeletal structure and differentiation.

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“…STAT-3 is phosphorylated at two different sites, tyrosine 705 and serine 727 [23]. The tyrosine kinase, JAK-1 phosphorylates STAT-3 at tyrosine 705 [24].…”

Section: Discussionmentioning

confidence: 99%

Correlation Analysis of JAK-STAT Pathway Components on Prognosis of Patients with Prostate Cancer

Liu

Li³

et al. 2011

Pathol. Oncol. Res.

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Janus kinases (JAK)/signal transducers and activator of transcription (STAT) pathway is activated constitutively in prostate cancer (PCa). Despite previous reports implying a role of this pathway in the development of clinical hormone-refractory PCa, the correlation of pathway members with the clinicopathologic features and prognosis of patients with PCa has not been elucidated. To address this problem, pJAK-1(Tyr1022/1023) and pSTAT-3(Tyr705) were evaluated by immunostaining in needle biopsies of the prostate from 202 PCa patients treated by definitive therapy (105 cases) or hormonal therapy (97 cases). The correlation of two protein expression with the clinicopathologic features and the prognosis of PCa were subsequently assessed. The expression levels of pJAK-1(Tyr1022/1023) and pSTAT-3(Tyr705) were both positively correlated with Gleason score and clinical stage of patients with PCa. Their expression was also significantly higher in patients with biochemical (prostate-specific antigen, PSA) failure than that in those with no PSA failure (both P < 0.001). In all patients, the recurrence-free survival (RFS) rates were significantly higher in those with low pJAK-1(Tyr1022/1023) and pSTAT-3(Tyr705) expression than that in those with high expression (both P < 0.001). Moreover, for patients treated by definitive or hormonal therapy, the RFS rates in those with lower pJAK-1(Tyr1022/1023) (P < 0.001 and 0.012, respectively) and pSTAT-3(Tyr705) expression (P < 0.001 and 0.015, respectively) were significantly higher than in those with higher expression. Cox multivariate analysis showed that the expression levels of pJAK-1(Tyr1022/1023) (P = 0.002) and pSTAT-3(Tyr705) (P = 0.005) were prognostic factors for PCa in addition to extraprostatic extension (P = 0.026) and Gleason score (P = 0.018). The results of pJAK-1(Tyr1022/1023) and pSTAT-3(Tyr705) immunostainings in needle-biopsy specimens are prognostic factors for PCa.

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Activation of JAK/STAT signal pathway predicts poor prognosis of patients with gliomas

Cited by 69 publications

References 29 publications

CUEDC2 suppresses glioma tumorigenicity by inhibiting the activation of STAT3 and NF-κB signaling pathway

CUEDC2 suppresses glioma tumorigenicity by inhibiting the activation of STAT3 and NF-κB signaling pathway

WWOX modulates the gene expression profile in the T98G glioblastoma cell line rendering its phenotype less malignant

Correlation Analysis of JAK-STAT Pathway Components on Prognosis of Patients with Prostate Cancer

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