Figure 5
Figure 5. Atiprimod-induced intracellular signaling and activation of the mitochondrial apoptotic cascades in MCL cells. Western blot analyses showing the protein levels in cells treated with atiprimod for different times: (A) Cytosolic (c) and total (t) AIF and cytochrome c. (B) MCL cell apoptosis induced by atiprimod in the presence or absence of AIF inhibitor (inh) N-phenylmaleimide and/or pan-caspase inhibitor Z-VAD (ZVAD). Apoptosis was detected by TUNEL assay. (C) Mitochondria-associated proapoptotic and antiapoptotic proteins, including Bax, Bcl-2, and phosphorylated (p) Bcl-2, Bcl-XL, and Bad. (D) JNK and phosphorylated JNK (pJNK), IκB and pIκB, STAT3, and pSTAT3 in MCL SP53 and Grant 519 cells. (E) JNK and pJNK in MCL Jeko-1 and MINO cells. MCL cells were incubated with 2 μM atiprimod for the indicated time points. Whole-cell lysates or cytosolic fractions were collected and subjected to Western blot analysis. Results of 3 independent experiments are shown (mean ± SE).

Atiprimod-induced intracellular signaling and activation of the mitochondrial apoptotic cascades in MCL cells. Western blot analyses showing the protein levels in cells treated with atiprimod for different times: (A) Cytosolic (c) and total (t) AIF and cytochrome c. (B) MCL cell apoptosis induced by atiprimod in the presence or absence of AIF inhibitor (inh) N-phenylmaleimide and/or pan-caspase inhibitor Z-VAD (ZVAD). Apoptosis was detected by TUNEL assay. (C) Mitochondria-associated proapoptotic and antiapoptotic proteins, including Bax, Bcl-2, and phosphorylated (p) Bcl-2, Bcl-XL, and Bad. (D) JNK and phosphorylated JNK (pJNK), IκB and pIκB, STAT3, and pSTAT3 in MCL SP53 and Grant 519 cells. (E) JNK and pJNK in MCL Jeko-1 and MINO cells. MCL cells were incubated with 2 μM atiprimod for the indicated time points. Whole-cell lysates or cytosolic fractions were collected and subjected to Western blot analysis. Results of 3 independent experiments are shown (mean ± SE).

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