cucurbitacin-d and 3-methyladenine

cucurbitacin-d has been researched along with 3-methyladenine* in 1 studies

Other Studies

1 other study(ies) available for cucurbitacin-d and 3-methyladenine

Article	Year
Autophagy is associated with cucurbitacin D-induced apoptosis in human T cell leukemia cells. Medical oncology (Northwood, London, England), 2016, Volume: 33, Issue:4 We previously reported that the inflammasome inhibitor cucurbitacin D (CuD) induces apoptosis in human leukemia cell lines. In the present study, we investigated the effects of co-treatment with an additional Bcl-xL inhibitor, Z36. Treatment with Z36 induced cell death in leukemia cell lines, with MT-4 cells exhibiting the lowest sensitivity to Z36. Co-treatment of cells with Z36 and CuD resulted in a greater degree of cell death for Hut78 and Jurkat cells than treatment with CuD alone. In contrast, co-treatment of MT-4 cells with Z36 and CuD had a suppressive effect on cell death. The autophagy inhibitor 3-methyladenine (3-MA) suppressed the growth of leukemia cell lines HuT78, Jurkat, MT-1, and MT-4. CuD-induced cell death was enhanced by 3-MA in Jurkat cells, but inhibited in MT-4 cells. Western blotting results revealed cleavage of poly(ADP ribose) polymerase (PARP), supporting CuD-induced cell death; 3-MA enhanced CuD-Z36-induced PARP cleavage. Taken together, our results indicate that autophagy negatively regulates chemical-induced cell death of leukemia cells, and that controlling autophagy could be beneficial in the development of more effective chemotherapies against leukemia. Topics: Adenine; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Autophagy; bcl-X Protein; Beclin-1; Cell Line, Tumor; Humans; Indoles; Jurkat Cells; Leukemia, T-Cell; Poly(ADP-ribose) Polymerases; Triterpenes	2016

Article

Year

Autophagy is associated with cucurbitacin D-induced apoptosis in human T cell leukemia cells.

Medical oncology (Northwood, London, England), 2016, Volume: 33, Issue:4

We previously reported that the inflammasome inhibitor cucurbitacin D (CuD) induces apoptosis in human leukemia cell lines. In the present study, we investigated the effects of co-treatment with an additional Bcl-xL inhibitor, Z36. Treatment with Z36 induced cell death in leukemia cell lines, with MT-4 cells exhibiting the lowest sensitivity to Z36. Co-treatment of cells with Z36 and CuD resulted in a greater degree of cell death for Hut78 and Jurkat cells than treatment with CuD alone. In contrast, co-treatment of MT-4 cells with Z36 and CuD had a suppressive effect on cell death. The autophagy inhibitor 3-methyladenine (3-MA) suppressed the growth of leukemia cell lines HuT78, Jurkat, MT-1, and MT-4. CuD-induced cell death was enhanced by 3-MA in Jurkat cells, but inhibited in MT-4 cells. Western blotting results revealed cleavage of poly(ADP ribose) polymerase (PARP), supporting CuD-induced cell death; 3-MA enhanced CuD-Z36-induced PARP cleavage. Taken together, our results indicate that autophagy negatively regulates chemical-induced cell death of leukemia cells, and that controlling autophagy could be beneficial in the development of more effective chemotherapies against leukemia.

Topics: Adenine; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Autophagy; bcl-X Protein; Beclin-1; Cell Line, Tumor; Humans; Indoles; Jurkat Cells; Leukemia, T-Cell; Poly(ADP-ribose) Polymerases; Triterpenes

2016