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SPOCD1 promotes the proliferation and metastasis of glioma cells by up-regulating PTX3.

ABSTRACT: Gliomas are the most prevalent type of primary brain tumors in adults, accounting for more than 40% of neoplasms in the central nervous system. The spen paralogue and orthologue C-terminal domain containing 1 (SPOCD1) has been recently identified and found to discriminate progressive from non-progressive bladder cancers. In this study, we detected high-level of SPOCD1 expression in glioma and its high expression significantly associated with advanced tumor grade and poor prognosis. In vitro assays showed that knockdown of SPOCD1 significantly inhibited cell proliferation and colony formation capacities in U373 and U87 cells. In a xenograft model of glioma, SPOCD1 was also found to inhibit tumor growth. In addition, knockdown of SPOCD1 was shown to inhibit cell migration and invasion in glioma U373 and U87 cells. SPOCD1 positively regulated the expression of Pentraxin 3 (PTX3), whereas overexpression of PTX3 attenuated SPOCD1 knockdown-mediated inhibition of cell proliferation, migration and invasion in glioma cells. Our observations suggest that SPOCD1 promotes the proliferation and metastasis of glioma cells through regulating PTX3. Our data might provide novel evidence for the diagnosis and treatment of glioma in clinic.

SUBMITTER: Liu Q

PROVIDER: S-EPMC5934553 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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SPOCD1 promotes the proliferation and metastasis of glioma cells by up-regulating PTX3.

Liu Quan Q Wang Xiao-Yu XY Qin Yuan-Yuan YY Yan Xian-Lei XL Chen Hong-Mou HM Huang Qi-Dan QD Chen Jia-Kang JK Zheng Jie-Min JM

American journal of cancer research 20180401 4

Gliomas are the most prevalent type of primary brain tumors in adults, accounting for more than 40% of neoplasms in the central nervous system. The spen paralogue and orthologue C-terminal domain containing 1 (SPOCD1) has been recently identified and found to discriminate progressive from non-progressive bladder cancers. In this study, we detected high-level of SPOCD1 expression in glioma and its high expression significantly associated with advanced tumor grade and poor prognosis. <i>In vitro</ ...[more]

PMID: 29736308

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Project description:Hematogenous metastasis requires tumor cells to detach from primary tumor into blood/lymphatic circulation and extravasate. Tumor cells in the blood circulation system, named circulating tumor cells (CTCs), are in a suspension state, with unique cytoskeletal structure and molecular phenotype different from primary tumor cells. The aim of this study is to assess the impact of suspension state on the metastatic potential of breast cancer cells (BCCs) and study its underlying mechanism. Methods: BCCs were cultured on low-adhesion plates to mimic the suspension state. Conventional adherent culture BCCs were used as the control. This study examined the metastatic potential of adherent and suspension BCCs in vitro and in vivo. RNA sequencing analysis, siRNA, and inhibitors were used to determine the underlying molecular mechanism. Results: The suspension state significantly increased the metastatic potential of BCCs, but slightly suppressed their tumor growth. RNA sequencing analysis revealed that the suspension state resulted in an acquisition of unique molecular signature enriched in pro-metastatic and tumor-suppressive genes. Specifically, prostaglandin-endoperoxide synthase 2 (PTGS2), which encodes protein cyclooxygenase-2 (COX-2), was identified as a highly up-regulated gene in suspension state compared with adherent cultured BCCs. Inhibition of the catalytic activity of COX-2 by celecoxib markedly suppressed suspension-increased migration and invasion of BCCs. In addition, knock-down of COX-2 by siRNA reduced the experimental lung metastasis formation of suspension cultured BCCs, which was associated with a remarkable decrease in retention and survival of BCCs in lungs of mice in the early stage of metastasis. Activation of Ca2+/calcineurin (CaN)/nuclear factor of activated T cells (NFAT) pathway and disruption of cytoskeleton contributed to the COX-2 up-expression by suspension state. Conclusions: Our results demonstrate that suspension state plays an important role in the metastatic potential of CTCs, and suggest a potential application of COX-2 inhibitor for anti-metastasis.

Dataset Information

SPOCD1 promotes the proliferation and metastasis of glioma cells by up-regulating PTX3.

Publications

SPOCD1 promotes the proliferation and metastasis of glioma cells by up-regulating PTX3.

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