Fig. 4. ERK signalling is uncoupled from cell cycle progression in Rb^-/- tumour cell lines. Asynchronously growing populations of tumour cells were plated at a density of 10⁴/ml. The following day cells were treated with U0126 at a final concentration of 20 µM, or vehicle control (DMSO). Growth of cells was monitored by BrdU incorporation 48 hour post treatment followed by immunofluorescence. (A) Proliferation of tumour cell lines derived from gliomas treated with inhibitor(s): SF295 (Rb wild-type) and SF539 (Rb deficient). (B) Proliferation of tumour cell lines derived from non-small lung carcinomas treated with inhibitor(s): H1299 (Rb wild-type) and H2009 (Rb deficient). (C) Inhibition of ERK activation by U0126.

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