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Fig. 5 | BMC Cancer

Fig. 5

From: An oncogenic mutant of RHEB, RHEB Y35N, exhibits an altered interaction with BRAF resulting in cancer transformation

Fig. 5

RHEB Y35N is Dependent on RAF/MEK/ERK Signaling, not mTORC1 Signaling, for Proliferation in Low Serum Conditions. (a) NIH 3T3 cell lines stably expressing RHEB WT, RHEB Y35N, or KRAS G12V as well as control were treated with 3 different concentrations of RAF/MEK/ERK inhibitor, U0126, for 48 h. % Viable Cells = (OD value of treated cells) / (OD value of non-treated cells) * 100. OD values were measured using Cell Counting Kit-8. Error bars represent standard deviation from three separate experiments, *p < 0.05, **p < 0.01, *** p < 0.001. The four cell lines grow similarly under normal condition as shown in Fig. 4a. b NIH 3T3 cell lines were grown in serum-free conditions, with or without 10 μM U0126 treatment. Growth was monitored using Cell Counting Kit-8 for 6 days. Error bars are shown from three repeated experiments (c) RHEB Y35N growth is not sensitive to mTORC1 inhibition. NIH 3T3 cell lines were treated with 3 different concentrations of mTORC1 inhibitor, Rapamycin, for 48 h. % Viable Cells and statistics calculated as in (a). d NIH 3T3 cell lines were grown in serum-free conditions, with or without 20 nM Rapamycin treatment. Growth was monitored as in (b)

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