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Figure 3 | Molecular Cancer

Figure 3

From: COX-2 inhibition is neither necessary nor sufficient for celecoxib to suppress tumor cell proliferation and focus formation in vitro

Figure 3

Increased expression of markers for ER stress and apoptosis in response to treatment with CXB, UMC, and DMC. U251 glioblastoma cells were treated with the indicated concentrations of CXB, UMC, and DMC and cell lysates were analyzed by Western blot with specific antibodies to CHOP (a pro-apoptotic ER stress indicator protein), cleaved (i.e., activated) caspase 7 (an ER stress-associated protein that participates in the execution of apoptosis), and PARP (proteolytic cleavage of PARP is executed by caspase 3 and indicates ongoing apoptosis). To verify equal loading in each case, the blots were also probed with an antibody to actin. The top panels represent lysates from cells treated with drugs for 18 hours (to reveal earlier events during ER stress). The bottom panels represent lysates from cells treated with drugs for 48 hours (to reveal later stages of ER stress-induced apoptosis). f.l.: full length PARP; cl.: cleaved PARP.

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