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Transcriptional co-activator TAZ sustains proliferation and tumorigenicity of neuroblastoma by targeting CTGF and PDGF-β.

Wang M, Liu Y, Zou J, Yang R, Xuan F, Wang Y, Gao N, Cui H - Oncotarget (2015)

Bottom Line: Here, we report that overexpression of TAZ in neuroblastoma BE(2)-C cells causes increases in cell proliferation, self renewal and colony formation, which was restored back to its original levels by knockdown of TAZ in TAZ-overexpression cells.Overall, our findings suggested that TAZ plays an essential role in regulating cell proliferation and tumorigenesis in neuroblastoma cells.Thus, TAZ seems to be a novel and promising target for the treatment of neuroblastoma.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.

ABSTRACT
Neuroblastoma is a common childhood malignant tumor originated from the neural crest-derived sympathetic nervous system. A crucial event in the pathogenesis of neuroblastoma is to promote proliferation of neuroblasts, which is closely related to poor survival. However, mechanisms for regulation of cell proliferation and tumorigenicity in neuroblastoma are not well understood. Here, we report that overexpression of TAZ in neuroblastoma BE(2)-C cells causes increases in cell proliferation, self renewal and colony formation, which was restored back to its original levels by knockdown of TAZ in TAZ-overexpression cells. Inhibition of endogenous TAZ attenuated cell proliferation, colony formation and tumor development in neuroblastoma SK-N-AS cell, which could be rescued by re-introduction of TAZ into TAZ-knockdown cells. In addition, we found that overexpressing TAZ-mediated induction of CTGF and PDGF-β expression, cell proliferation and colony formation were inhibited by knocking down CTGF and PDGF-β with siRNA in TAZ-overexpressing cell. Overall, our findings suggested that TAZ plays an essential role in regulating cell proliferation and tumorigenesis in neuroblastoma cells. Thus, TAZ seems to be a novel and promising target for the treatment of neuroblastoma.

No MeSH data available.


Related in: MedlinePlus

TAZ expression is prognostic of worse survival in neuroblastoma patients(A) Kaplan-Meier analysis of progression-free survival for Versteeg dataset with log-rank test P-values indicated. The TAZ expression cutoff value 0.035 was determined by the online R2: microarray analysis and visualization platform, which separated patients into high and low TAZ expression groups. (B) Kaplan-Meier analysis of the Seeger dataset with the log-rank test P value indicated. (C) Box plot of TAZ expression levels in tumor good and poor prognosis groups.
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Figure 1: TAZ expression is prognostic of worse survival in neuroblastoma patients(A) Kaplan-Meier analysis of progression-free survival for Versteeg dataset with log-rank test P-values indicated. The TAZ expression cutoff value 0.035 was determined by the online R2: microarray analysis and visualization platform, which separated patients into high and low TAZ expression groups. (B) Kaplan-Meier analysis of the Seeger dataset with the log-rank test P value indicated. (C) Box plot of TAZ expression levels in tumor good and poor prognosis groups.

Mentions: To investigate the prognostic value of TAZ in neuroblastoma, the Tumor Neuroblastoma public-Versteeg database, which is available from the online R2: microarray analysis and visualization platform were performed. The Versteeg database contains a cohort of 88 patients with neuroblastoma representative of survival prognosis. 71 patients with high TAZ expression showed low survival probability, whereas 17 patients with low TAZ expression showed high survival probability (Figure 1A), suggesting that high TAZ expression is prognostic for poor outcome of neuroblastoma patients. Kaplan-Meier analysis of progression-free survival for the Seeger dataset also confirmed that high TAZ expression was associated with poor outcome, whereas low TAZ expression was associated with good prognosis (Figure 1B and 1C). Together, our analysis of two independent datasets indicated that TAZ could be a potential prognostic marker in neuroblastoma.


Transcriptional co-activator TAZ sustains proliferation and tumorigenicity of neuroblastoma by targeting CTGF and PDGF-β.

Wang M, Liu Y, Zou J, Yang R, Xuan F, Wang Y, Gao N, Cui H - Oncotarget (2015)

TAZ expression is prognostic of worse survival in neuroblastoma patients(A) Kaplan-Meier analysis of progression-free survival for Versteeg dataset with log-rank test P-values indicated. The TAZ expression cutoff value 0.035 was determined by the online R2: microarray analysis and visualization platform, which separated patients into high and low TAZ expression groups. (B) Kaplan-Meier analysis of the Seeger dataset with the log-rank test P value indicated. (C) Box plot of TAZ expression levels in tumor good and poor prognosis groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4496235&req=5

Figure 1: TAZ expression is prognostic of worse survival in neuroblastoma patients(A) Kaplan-Meier analysis of progression-free survival for Versteeg dataset with log-rank test P-values indicated. The TAZ expression cutoff value 0.035 was determined by the online R2: microarray analysis and visualization platform, which separated patients into high and low TAZ expression groups. (B) Kaplan-Meier analysis of the Seeger dataset with the log-rank test P value indicated. (C) Box plot of TAZ expression levels in tumor good and poor prognosis groups.
Mentions: To investigate the prognostic value of TAZ in neuroblastoma, the Tumor Neuroblastoma public-Versteeg database, which is available from the online R2: microarray analysis and visualization platform were performed. The Versteeg database contains a cohort of 88 patients with neuroblastoma representative of survival prognosis. 71 patients with high TAZ expression showed low survival probability, whereas 17 patients with low TAZ expression showed high survival probability (Figure 1A), suggesting that high TAZ expression is prognostic for poor outcome of neuroblastoma patients. Kaplan-Meier analysis of progression-free survival for the Seeger dataset also confirmed that high TAZ expression was associated with poor outcome, whereas low TAZ expression was associated with good prognosis (Figure 1B and 1C). Together, our analysis of two independent datasets indicated that TAZ could be a potential prognostic marker in neuroblastoma.

Bottom Line: Here, we report that overexpression of TAZ in neuroblastoma BE(2)-C cells causes increases in cell proliferation, self renewal and colony formation, which was restored back to its original levels by knockdown of TAZ in TAZ-overexpression cells.Overall, our findings suggested that TAZ plays an essential role in regulating cell proliferation and tumorigenesis in neuroblastoma cells.Thus, TAZ seems to be a novel and promising target for the treatment of neuroblastoma.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.

ABSTRACT
Neuroblastoma is a common childhood malignant tumor originated from the neural crest-derived sympathetic nervous system. A crucial event in the pathogenesis of neuroblastoma is to promote proliferation of neuroblasts, which is closely related to poor survival. However, mechanisms for regulation of cell proliferation and tumorigenicity in neuroblastoma are not well understood. Here, we report that overexpression of TAZ in neuroblastoma BE(2)-C cells causes increases in cell proliferation, self renewal and colony formation, which was restored back to its original levels by knockdown of TAZ in TAZ-overexpression cells. Inhibition of endogenous TAZ attenuated cell proliferation, colony formation and tumor development in neuroblastoma SK-N-AS cell, which could be rescued by re-introduction of TAZ into TAZ-knockdown cells. In addition, we found that overexpressing TAZ-mediated induction of CTGF and PDGF-β expression, cell proliferation and colony formation were inhibited by knocking down CTGF and PDGF-β with siRNA in TAZ-overexpressing cell. Overall, our findings suggested that TAZ plays an essential role in regulating cell proliferation and tumorigenesis in neuroblastoma cells. Thus, TAZ seems to be a novel and promising target for the treatment of neuroblastoma.

No MeSH data available.


Related in: MedlinePlus