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M2 receptor activation inhibits cell cycle progression and survival in human glioblastoma cells.

Ferretti M, Fabbiano C, Di Bari M, Conte C, Castigli E, Sciaccaluga M, Ponti D, Ruggieri P, Raco A, Ricordy R, Calogero A, Tata AM - J. Cell. Mol. Med. (2013)

Bottom Line: Cell growth analysis has demonstrated that the M2 agonist arecaidine strongly decreased cell proliferation in both glioma cell lines and primary cultures.This effect was dose and time dependent.Chemosensitivity assays have, moreover, shown arecaidine and temozolomide similar effects on glioma cell lines, although IC50 value for arecaidine was significantly lower than temozolomide.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology and Biotechnologies Charles Darwin, Research Centre of Neurobiology Daniel Bovet, La Sapienza, University of Rome, P.le Aldo Moro, 5-00185 Roma, Italy.

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Effect of arecaidine on primary cell lines obtained from biopsies. Time and dose dependent analysis of cell growth by different doses of arecaidine (10–100 μM) has been evaluated in five different primary cell cultures (MTZ, CRL-8, BLO, FCN-9, MZC-12). Data are the mean ± SEM of three independent experiments performed in triplicate. (DIV: day in vitro).
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fig04: Effect of arecaidine on primary cell lines obtained from biopsies. Time and dose dependent analysis of cell growth by different doses of arecaidine (10–100 μM) has been evaluated in five different primary cell cultures (MTZ, CRL-8, BLO, FCN-9, MZC-12). Data are the mean ± SEM of three independent experiments performed in triplicate. (DIV: day in vitro).

Mentions: All primary cell cultures and stable cell lines showed a significant decrease in cell proliferation in presence of 100 μM arecaidine and 10% FCS (P < 0.001, arecaidine versus control; Fig. 4). The most sensitive were CRL-8, MTR, BML and U251 cell lines indicating that the efficacy of arecaidine is independent of gene status. Comparable results were obtained in presence of low concentrations of FCS (data not shown).


M2 receptor activation inhibits cell cycle progression and survival in human glioblastoma cells.

Ferretti M, Fabbiano C, Di Bari M, Conte C, Castigli E, Sciaccaluga M, Ponti D, Ruggieri P, Raco A, Ricordy R, Calogero A, Tata AM - J. Cell. Mol. Med. (2013)

Effect of arecaidine on primary cell lines obtained from biopsies. Time and dose dependent analysis of cell growth by different doses of arecaidine (10–100 μM) has been evaluated in five different primary cell cultures (MTZ, CRL-8, BLO, FCN-9, MZC-12). Data are the mean ± SEM of three independent experiments performed in triplicate. (DIV: day in vitro).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3822656&req=5

fig04: Effect of arecaidine on primary cell lines obtained from biopsies. Time and dose dependent analysis of cell growth by different doses of arecaidine (10–100 μM) has been evaluated in five different primary cell cultures (MTZ, CRL-8, BLO, FCN-9, MZC-12). Data are the mean ± SEM of three independent experiments performed in triplicate. (DIV: day in vitro).
Mentions: All primary cell cultures and stable cell lines showed a significant decrease in cell proliferation in presence of 100 μM arecaidine and 10% FCS (P < 0.001, arecaidine versus control; Fig. 4). The most sensitive were CRL-8, MTR, BML and U251 cell lines indicating that the efficacy of arecaidine is independent of gene status. Comparable results were obtained in presence of low concentrations of FCS (data not shown).

Bottom Line: Cell growth analysis has demonstrated that the M2 agonist arecaidine strongly decreased cell proliferation in both glioma cell lines and primary cultures.This effect was dose and time dependent.Chemosensitivity assays have, moreover, shown arecaidine and temozolomide similar effects on glioma cell lines, although IC50 value for arecaidine was significantly lower than temozolomide.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology and Biotechnologies Charles Darwin, Research Centre of Neurobiology Daniel Bovet, La Sapienza, University of Rome, P.le Aldo Moro, 5-00185 Roma, Italy.

Show MeSH
Related in: MedlinePlus