Figure 4
Atg7 knockdown abrogates marrow/stroma-induced chemoprotection and enhances susceptibility to chemotherapeutic stress. OCI-AML3 cells (ShControl or ShAtg7) were cultured with (A) monolayer of normal bone marrow–derived stromal cells or (B) stromal cells (ShControl or ShAtg7) and treated with Ara-C (2 μM) and Ida (5 ng/mL) for 72 hours, and apoptosis was assessed by annexin V binding (flow cytometry). Lysates were immunoblotted to Atg7 and β-actin to confirm knockdown of Atg7 and loading control, respectively (box). Duplicate whole cell lysates were separated on SDS-polyacrylamide gel electrophoresis and probed with LC3 and p62. β-Actin was used as loading control (bottom panel).

Atg7 knockdown abrogates marrow/stroma-induced chemoprotection and enhances susceptibility to chemotherapeutic stress. OCI-AML3 cells (ShControl or ShAtg7) were cultured with (A) monolayer of normal bone marrow–derived stromal cells or (B) stromal cells (ShControl or ShAtg7) and treated with Ara-C (2 μM) and Ida (5 ng/mL) for 72 hours, and apoptosis was assessed by annexin V binding (flow cytometry). Lysates were immunoblotted to Atg7 and β-actin to confirm knockdown of Atg7 and loading control, respectively (box). Duplicate whole cell lysates were separated on SDS-polyacrylamide gel electrophoresis and probed with LC3 and p62. β-Actin was used as loading control (bottom panel).

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