Interplay of apoptosis and autophagy in acute lymphoblastic leukemia cells

Includes bibliographical references (pages 70-75)Apoptosis and Autophagy are two processes that play key roles in the death and survival of cells. Apoptosis is a cell death mechanism, where autophagy is a cell survival as well as a cell death mechanism. In this study we investigated whether and how these two processes interact with each other in human lymphoblastic leukemic cells. Two cell lines were used: the first being CEM C1-15, resistant to dexamethasone-induced apoptotic death. The second cell line being CEM C7-14, sensitive to dexamethasone-induced death. The drug reagent rapamycin, an mTOR inhibitor, was utilized to induce autophagy. Dexamethasone, a synthetic glucocorticoid, was used to induce Apoptosis. Additionally, 3-Methyl Adenine (3MA) was employed to rescue cells from an autophagic fate caused by rapamycin. We show that apoptosis and autophagy collaborate in CEM C1-15 and C7-14 cells, and are able to take place simultaneously in the same cell. We also show that there is a synergistic effect when both processes are induced, resulting in a stronger death response. Moreover, we have used cell growth assay data in conjunction with fluorescent microscopy images to show that when autophagy is inhibited, apoptosis takes over as the primary cell death mechanism. In summary, our results add to the knowledge of apoptotic-autophagic interaction in leukemic cells and show that epifluorescence microscopy is a useful tool in aiding researchers to take specific and detailed images of cellular processes