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// Mei Wang 1, * , Yang Liu 2, 3, * , Jiahua Zou 1 , Rui Yang 1 , Fan Xuan 1 , Yi Wang 3 , Ning Gao 4 , Hongjuan Cui 1 1 State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China 2 Department of Respiration, the Third Hospital of Hebei Medical University, Shijiazhuang, China 3 Cardiovascular Department, Second Affiliated Hospital of University of South China, Hengyang, China 4 Department of Pharmacognosy, College of Pharmacy, Third Military Medical University, Chongqing, China * These authors have contributed equally to this work Correspondence to: Hongjuan Cui, e-mail: hongjuan.cui@gmail.com , hcui@swu.edu.cn Ning Gao, e-mail: gaoning59@gmail.com Keywords: TAZ, cell proliferation, colony formation, neuroblastoma Received: Novmember 25, 2014 Accepted: February 11, 2015 Published: March 24, 2015 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.

Osteosarcoma is the most common primary malignant bone tumor in adolescents and young adults. However, the involvement of serine/threonine phosphatase type 5 (PP5) in osteosarcoma remains unclear. The aim of this study was to evaluate the functional role of PP5 in osteosarcoma cells. Firstly, we found that PP5 is widely expressed in several human osteosarcoma cell lines. Then we used lentivirus-delivered siRNA to silence PP5 expression in Saos-2 and U2OS cell lines. Knockdown of endogenous PP5 expression by shRNA-expressing lentivirus significantly decreased the viability and proliferation of the osteosarcoma cells. Moreover, FACS analysis showed that knockdown of PP5 expression induced a significant arrest in the G0/G1 phase of the cell cycle, which was associated with the inhibition of cell proliferation. Therefore, knockdown of PP5 is likely to provide a novel alternative to targeted therapy of osteosarcoma and deserves further investigation.