Vitamin D compounds. Effect on clonal proliferation and differentiation of human myeloid cells.

Munker, Reinhold; Norman, Anthony W.; Koeffler, H. Phillip

doi:10.1172/jci112593

Cited by 178 publications

(80 citation statements)

References 27 publications

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“…For clonogenic assays, cells were plated into 24-well flat-bottomed plates using a two-layer soft agar system with a total of 3 3 10 3 cells/well in a volume of 400 ll/well, as described previously. 10 After 10 days of incubation, the colonies were counted. For proliferation measurements, the cells were placed into 96 well plates, and cell growth was measured at various times by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay according to the protocol provided by Roche Molecular Biochemicals (Basel, Switzerland).…”

Section: Glioma Cell Lines Cell Proliferation and Migrationmentioning

confidence: 99%

Cucurbitacin B markedly inhibits growth and rapidly affects the cytoskeleton in glioblastoma multiforme

Ding

Wakimoto

Xing

et al. 2008

Intl Journal of Cancer

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Glioblastoma Multiforme (GBM) is almost inevitably a fatal tumor of the brain with most individuals dying within 1 year of diagnosis. It is the most frequent brain tumor in adults. Dose-response studies showed that Cucurbitacin B inhibited 50% growth (ED 50 ) of 5 human GBM cell lines in liquid culture at 10 27 M. Soft-gel assays demonstrated that nearly all of the GBM clonogenic cells were inhibited at 10 28 M of Cucurbitacin B. FACS analysis found that the compound (10 27 M, 24 hr) caused G2/M arrest. The GBM cells underwent profound morphologic changes within 15-30 min after exposure to Cucurbitacin B (10 27 M), rounding up and losing their pseudopodia associated with disruption of actin and microtubules, as observed by immunoflourescence. Cucurbitacin B (10 27 M) caused prominent multinucleation of the cells after they were pulse-exposed (48 hr) to the drug, washed and cultured in normal medium for an additional 2 days. The drug (10 27 M, 3-24 hr) increased levels of p-p38, p-JNK and p-JUN in U87 and T98G GBM cell lines as seen by Western blot. Interestingly, alterations in cell morphology caused by Cucurbitacin B (10 27 M) were blocked by the JNK inhibitor SP600125. In summary, Cucurbitacin B has a prominent anti-proliferative activity on GBM cells; and at least in part, the mode of action is by affecting the cytoskeleton, as well as, the JNK pathway. Clinical trails of this drug should be pursued in GBM.

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Section: Glioma Cell Lines Cell Proliferation and Migrationmentioning

confidence: 99%

Cucurbitacin B markedly inhibits growth and rapidly affects the cytoskeleton in glioblastoma multiforme

Ding

Wakimoto

Xing

et al. 2008

Intl Journal of Cancer

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“…Cells were plated in 24-well flat-bottomed plates using a two-layer soft agar system with 1 Â 10 3 cells per well in a volume of 400 ml per well as described earlier (Munker et al, 1986). After 14 days of incubation, colonies were counted and measured.…”

Section: Soft Agar Assaymentioning

confidence: 99%

Involvement of Cyr61 in growth, migration, and metastasis of prostate cancer cells

et al. 2008

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Cyr61 has been reported to participate in the development and progression of various cancers; however, its role in prostate cancer (PCa) still remains poorly understood. In this study, we explored the function of Cyr61 in a series of malignant PCa cell lines, including LnCap, Du145, and PC3. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and crystal violet assays demonstrated that Cyr61 was essential for the proliferation of PCa cells. Soft agar assay and xenograft analysis showed that downregulation of Cyr61 suppressed the tumorigenicity of Du145 cells both in vitro and in vivo. Either silencing the cellular Cyr61 by RNA interference or neutralising the endogenous Cyr61 by antibody inhibited the migration of Du145 cells. In contrast, purified protein of Cyr61 promoted the migration of LnCap cells in a dose-dependent manner. These results suggested that Cyr61 was involved in the migration of PCa cells. We also observed the accumulation of mature focal adhesion complexes associated with the impaired migration through Cyr61 downregulation. Also, further studies showed that Cyr61 regulated the level of activated Rac1 as well as its downstream targets, including phosphorylated JNK, E-cadherin, and p27 kip1 , which are key molecules involved in cell growth, migration, and invasion. The in vivo mouse tail vein injection experiment revealed that Cyr61 affected the metastatic capacity of Du145 cells, suggesting that Cyr61 was required for prostate tumour metastasis. Altogether, our results demonstrated that Cyr61 played an important role in the tumorigenicity and metastasis of PCa cells, which will benefit the development of therapeutic strategy for PCas.

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“…The selected clones were confirmed by Western blot analysis. For clonogenic assays, cells were plated into 24-well flat-bottomed plates using a two-layer soft agar system with a total of 1 Â 10 3 cells/well in a volume of 400 ml/well, as described previously (Munker et al, 1986). After 14 days of incubation, the colonies were counted.…”

Section: Cell Transfection and Soft Agar Assaysmentioning

confidence: 99%

DLK1: increased expression in gliomas and associated with oncogenic activities

et al. 2006

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DLK1 (delta-like) is a transmembrane and secreted protein in the epidermal growth factor-like homeotic family. Although expressed widely during embryonic development, only a few tissues retain the expression in adults. Neuroendocrine tumors often highly express this protein; therefore, we hypothesized that brain tumors might also express it. This study found that the expression of DLK1 in gliomas was higher than that in normal brain (Po0.05). After stable transfection of a DLK1 cDNA expression vector into GBM cell lines, their proliferation was increased. Furthermore, they lost contact inhibition, had enhanced anchorage-independent growth in soft agar, and had significantly greater capacity to migrate. Western blot studies showed that expression of cyclin D1, CDK2, and E2F4 were increased, and Rb levels were decreased in these cells. DLK1 was found on the cell surface and secreted in the medium from the transfected GBM cells. DLK1-enriched condition medium stimulated the growth of glioblastoma multiforme cell lines and explants. DLK1 antibody blocked cell growth stimulated by DLK1. In summary, these results suggest that DLK1 may play a role in the formation or progression of gliomas.

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Vitamin D compounds. Effect on clonal proliferation and differentiation of human myeloid cells.

Cited by 178 publications

References 27 publications

Cucurbitacin B markedly inhibits growth and rapidly affects the cytoskeleton in glioblastoma multiforme

Cucurbitacin B markedly inhibits growth and rapidly affects the cytoskeleton in glioblastoma multiforme

Involvement of Cyr61 in growth, migration, and metastasis of prostate cancer cells

DLK1: increased expression in gliomas and associated with oncogenic activities

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