aag treatment  (Cell Signaling Technology Inc)

Journal: Cell cycle (Georgetown, Tex.)

Article Title: Cancer cells harboring MET gene amplification activate alternative signaling pathways to escape MET inhibition but remain sensitive to Hsp90 inhibitors

doi: 10.4161/cc.8.13.8861

Figure Lengend Snippet: Effects of c-Met TKI and Hsp90 inhibitor on induction of apoptosis. (A) H1993 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using PARP antibody (lower band represents the cleaved PARP) and cleaved Caspase-3 antibody. α-tubulin was used as a loading control. (B) H1993 cells were treated with SU11274 or 17-AAG for the indicated times. Cells were stained with propidium iodide, and the extent of apoptosis was calculated as described in Methods.

Article Snippet: As in H1993 cells, 17-AAG treatment resulted in robust and durable inhibition of each of these parameters. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 5. caption a7 Effects of c-Met TKI and Hsp90 inhibitor on cell signaling and proliferation of MKN45 cells. (A) MKN45 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using specific antibodies. (B) MKN45 cells were treated with SU11274 for 4 h (lane 2) or 96 h (lane 3–5).

Techniques: Western Blot, Staining

Journal: Cell cycle (Georgetown, Tex.)

Article Title: Cancer cells harboring MET gene amplification activate alternative signaling pathways to escape MET inhibition but remain sensitive to Hsp90 inhibitors

doi: 10.4161/cc.8.13.8861

Figure Lengend Snippet: Effects of c-Met TKI and Hsp90 inhibitor on Akt and Erk signaling. H1993 cells were treated with SU11274 or 17-AAG for the indicated times and lysates were immunoblotted as shown. ‘C’ = untreated cells.

Article Snippet: As in H1993 cells, 17-AAG treatment resulted in robust and durable inhibition of each of these parameters. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 5. caption a7 Effects of c-Met TKI and Hsp90 inhibitor on cell signaling and proliferation of MKN45 cells. (A) MKN45 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using specific antibodies. (B) MKN45 cells were treated with SU11274 for 4 h (lane 2) or 96 h (lane 3–5).

Techniques:

Journal: Cell cycle (Georgetown, Tex.)

Article Title: Cancer cells harboring MET gene amplification activate alternative signaling pathways to escape MET inhibition but remain sensitive to Hsp90 inhibitors

doi: 10.4161/cc.8.13.8861

Figure Lengend Snippet: Involvement of PKC δ in the reactivation of EGFR family members and downstream Akt and Erk signaling following prolonged c-Met TKI treatment. (A) H1993 cells were treated with SU11274 or 17-AAG for the indicated times and analyzed by immunoblotting using anti-PKC δ or anti-PKC δ (pS664) antibodies. Tubulin was used as a loading control. (B) H1993 cells were treated with SU1274 for 4 h (lane 2) or 48 h (lane 3–6). CI-1033 (1.5 μM, lane 4), rottlerin (10 μM, lane 5), or GO6976 (10 μM, lane 6) were added 4 hours before the cells were harvested. Untreated (lane 1) or treated cells were analyzed by immunobloting with the indicated antibodies. (C) H1993 cells were incubated continuously with DMSO (◆), CI-1033 (1.5 μM, ∎), SU11274 (2.5 μM, ▴), 17-AAG (0.5 μM, *), SU11274 and CI-1033 (◻), or SU11274 and rottlerin (1 μM, ▵). Cell density was monitored for 6 consecutive days by MTS assay. Each point represents the mean of 4 determinations; error bars, SD.

Article Snippet: As in H1993 cells, 17-AAG treatment resulted in robust and durable inhibition of each of these parameters. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 5. caption a7 Effects of c-Met TKI and Hsp90 inhibitor on cell signaling and proliferation of MKN45 cells. (A) MKN45 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using specific antibodies. (B) MKN45 cells were treated with SU11274 for 4 h (lane 2) or 96 h (lane 3–5).

Techniques: Western Blot, Incubation, MTS Assay

Journal: Cell cycle (Georgetown, Tex.)

Article Title: Cancer cells harboring MET gene amplification activate alternative signaling pathways to escape MET inhibition but remain sensitive to Hsp90 inhibitors

doi: 10.4161/cc.8.13.8861

Figure Lengend Snippet: Effects of c-Met TKI and Hsp90 inhibitor on cell signaling and proliferation of MKN45 cells. (A) MKN45 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using specific antibodies. (B) MKN45 cells were treated with SU11274 for 4 h (lane 2) or 96 h (lane 3–5). Rottlerin (10 μM) was added for 4 h (lane 4) or 96 h (lane 5). Cell lysates were analyzed by immunobloting with the indicated antibodies. (C) MKN45 cells were incubated continuously with DMSO (◆), SU11274 (▴), 17-AAG (◻) or SU11274 and rottlerin (*), and cell proliferation was monitored by MTS assay. Each point represents the mean of 4 determinations; error bars, SD.

Article Snippet: As in H1993 cells, 17-AAG treatment resulted in robust and durable inhibition of each of these parameters. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 5. caption a7 Effects of c-Met TKI and Hsp90 inhibitor on cell signaling and proliferation of MKN45 cells. (A) MKN45 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using specific antibodies. (B) MKN45 cells were treated with SU11274 for 4 h (lane 2) or 96 h (lane 3–5).

Techniques: Western Blot, Incubation, MTS Assay