Elevated Cell Invasion in a Tumor Sphere Culture of RSV-M Mouse Glioma Cells

Nonaka, Motonobu; Yawata, Toshio; Takemura, Mitsuhiro; Higashi, Yoshitaka; Nakai, Eiichi; Shimizu, Katsuji; Ueba, Tetsuya

doi:10.2176/nmc.oa.2014-0067

Cited by 10 publications

(7 citation statements)

References 47 publications

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“…The secondary and tertiary rounds of tumor sphere culture were similary conducted after harvesting the first round of tumor sphere culture cells. At the end of each round of culture, the number and size of tumor spheres were determined 58 .…”

Section: Methodsmentioning

confidence: 99%

Class III-specific HDAC inhibitor Tenovin-6 induces apoptosis, suppresses migration and eliminates cancer stem cells in uveal melanoma

Dai

Zhou

Jin

et al. 2016

Sci Rep

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Uveal melanoma (UM) is the most common intraocular malignancy in adults. Despite improvements in surgical, radiation and chemotherapy treatments, the overall survival of UM and prognosis remain poor. In the present study, we hypothesized that Sirtuin 1 and 2 (SIRT1/2), class III histone deacetylases (HDACs), were critical in controlling the destiny of bulk tumor cells and cancer stem cells (CSCs) of UM. We testified this hypothesis in four lines of UM cells (92.1, Mel 270, Omm 1 and Omm 2.3). Our results showed that inhibition of SIRT1/2 by Tenovin-6 induced apoptosis in UM cells by activating the expression of tumor suppressor genes such as p53 and elevating reactive oxygen species (ROS). Tenovin-6 inhibited the growth of UM cells. Tenovin-6 and vinblastine was synergistic in inducing apoptosis of UM cell line 92.1 and Mel 270. Furthermore, Tenovin-6 eliminated cancer stem cells in 92.1 and Mel 270 cells. In conclusion, our findings suggest that Tenovin-6 may be a promising agent to kill UM bulk tumor cells and CSCs.

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Section: Methodsmentioning

confidence: 99%

Class III-specific HDAC inhibitor Tenovin-6 induces apoptosis, suppresses migration and eliminates cancer stem cells in uveal melanoma

Dai

Zhou

Jin

et al. 2016

Sci Rep

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“…We have also demonstrated that tumorspheres derived from HNSCC cells displayed EMT signatures such as low expression of epithelial marker E-cadherin and high expression of mesenchymal markers such as vimentin, Slug and zinc finger E-box-binding homeobox 1 (ZEB1) [ 63 ]. Nonaka et al found an elevated invasive ability in tumorspheres derived from RSV-M mouse glioma cells associated with the differential expression of metastatic genes [ 64 ]. In addition, tumor cells from metastatic site have been reported to be more easily engrafted in immunocompromised mice than those from the primary site.…”

Section: Tumorspheres Display All the Characteristics Of Cancer Stem mentioning

confidence: 99%

Tumorsphere as an effectivein vitroplatform for screening anti-cancer stem cell drugs

et al. 2015

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Cancer stem cells (CSCs) are a sub-population of cells within cancer tissues with tumor initiation, drug resistance and metastasis properties. CSCs also have been considered as the main cause of cancer recurrence. Targeting CSCs have been suggested as the key for successful treatment against cancer. Tumorsphere cultivation is based on culturing cancer cells onto ultralow attachment surface in serum-free media under the supplementation with growth factors such as epidermal growth factor and basic fibroblast growth factor. Tumorsphere cultivation is widely used to analyze the self-renewal capability of CSCs and to enrich these cells from bulk cancer cells. This method also provides a reliable platform for screening potential anti-CSC agents. The in vitro anti-proliferation activity of potential agents selected from tumorsphere assay is more translatable into in vivo anti-tumorigenic activity compared with general monolayer culture. Tumorsphere assay can also measure the outcome of clinical trials for potential anti-cancer agents. In addition, tumorsphere assay may be a promising strategy in the innovation of future cancer therapeutica and may help in the screening of anti-cancer small-molecule chemicals.

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“…92.1 and Omm 1 cells pretreated with DMSO or 1.0 µM pristimerin for 24 h were seeded to 24-well low attachment plates containing 500 µl DMEM/F12 medium supplemented with 1X B27, 10 ng/ml basic fibroblast growth factor (bFGF), 20 ng/ml epidermal growth factor (EGF) each well. After ~14 days, melanospheres with >50 cells were counted as per the universal standard (29,36). The secondary and tertiary rounds of melanosphere cultures were implemented in drug-free culture after collecting the first or second round of tumor sphere culture cells.…”

Section: Preparation Of Whole Cell Lysates and Cytosolic Fractionationsmentioning

confidence: 99%

Pristimerin effectively inhibits the malignant phenotypes of uveal melanoma cells by targeting NF-κB pathway

Zhang

Pan

2017

International Journal of Oncology

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Uveal melanoma (UM) is a highly aggressive intraocular malignancy that lacks any effective targeted-therapy. Neither survival nor prognosis has been improved for the past decades in patients with metastatic UM. NF‑κB pathway is reported to be abnormally activated in UM. However, the role of NF‑κB pathway as a potential therapeutical target in UM remains unclear. Here, the effect of pristimerin, a potent inhibitor of NF‑κB pathway, on UM cells in terms of growth, apoptosis, motility, invasion and cancer stem-like cells (CSCs) was evaluated in vitro. We showed that pristimerin suppressed tumor necrosis factor α (TNFα)-induced IκBα phosphorylation, translocation of p65, and expression of NF‑κB-dependent genes. Moreover, pristimerin decreased cell viability and clonogenic ability of UM cells. A synergistic effect was observed in the treatment of pristimerin combined with vinblastine, a frontline therapeutic agent, in UM. Pristimerin led to a significant increase in the Annexin V+ cell population as measured by flow cytometry. We also observed that pristimerin impaired the abilities of migration and invasion in UM cells. Furthermore, pristimerin eliminated the ALDH+ cells and weakened serial re-plating ability of melanosphere. Collectively, pristimerin shows remarkable anticancer activities in UM cells through inactivating NF‑κB pathway, revealing that pristimerin may be a promising therapeutic agent in UM.

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Elevated Cell Invasion in a Tumor Sphere Culture of RSV-M Mouse Glioma Cells

Cited by 10 publications

References 47 publications

Class III-specific HDAC inhibitor Tenovin-6 induces apoptosis, suppresses migration and eliminates cancer stem cells in uveal melanoma

Class III-specific HDAC inhibitor Tenovin-6 induces apoptosis, suppresses migration and eliminates cancer stem cells in uveal melanoma

Tumorsphere as an effectivein vitroplatform for screening anti-cancer stem cell drugs

Pristimerin effectively inhibits the malignant phenotypes of uveal melanoma cells by targeting NF-κB pathway

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