Autophagy in tumour cell death

Macintosh, Robin L.; Ryan, Kevin M.

doi:10.1016/j.semcancer.2013.05.006

Cited by 110 publications

(97 citation statements)

References 98 publications

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“…Furthermore, autophagy-related ULK-1 and DRAM genes were significantly upregulated in cells treated with AMG 232 and radiation. Although autophagy is often considered to be a cell survival mechanism, there is also evidence for the capacity of autophagy to mediate the antiproliferative and/or cytotoxic actions of selected anticancer agents (31,32). Furthermore, a direct crosstalk between apoptosis and autophagy has been identified that serves to reinforce cell death (33).…”

Section: Discussionmentioning

confidence: 99%

Small Molecule Inhibition of MDM2–p53 Interaction Augments Radiation Response in Human Tumors

Werner

Huang

Francis

et al. 2015

Molecular Cancer Therapeutics

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MDM2-p53 interaction and downstream signaling affect cellular response to DNA damage. AMG 232 is a potent small molecule inhibitor that blocks the interaction of MDM2 and p53. We examined the capacity of AMG 232 to augment radiation response across a spectrum of human tumor cell lines and xenografts. AMG 232 effectively inhibited proliferation and enhanced radiosensitivity via inhibition of damage repair signaling. Combined AMG 232 and radiation treatment resulted in the accumulation of gH2AX-related DNA damage and induction of senescence with promotion of apoptotic and/ or autophagic cell death. Several molecules involved in senescence, autophagy, and apoptosis were specifically modulated following the combined AMG 232/radiation treatment, including FoxM1, ULK-1, DRAM, and BAX. In vivo xenograft studies confirmed more potent antitumor and antiangiogenesis efficacy with combined AMG 232/radiation treatment than treatment with drug or radiation alone. Taken together, these data identify the capacity of AMG 232 to augment radiation response across a variety of tumor types harboring functional p53.

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Section: Discussionmentioning

confidence: 99%

Small Molecule Inhibition of MDM2–p53 Interaction Augments Radiation Response in Human Tumors

Werner

Huang

Francis

et al. 2015

Molecular Cancer Therapeutics

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“…75 Furthermore, autophagy may be activated in tumor cells in response to a variety of anticancer therapies. [128][129][130][131] Autophagy confers resistance to therapy, and the inhibition of autophagy sensitizes tumor cells to cell death induced by several anticancer treatments. 129 In the presence of certain anticancer agents, however, the induction of autophagy results in synergistic antitumor effects.…”

Section: Targeting Glutaminolysis and Autophagy As An Anticancer Therapymentioning

confidence: 99%

“…129 In the presence of certain anticancer agents, however, the induction of autophagy results in synergistic antitumor effects. 130,131 Thus, autophagy can be considered as a double-edged sword in tumorigenesis and cancer therapy. Given the important functions of autophagy in cancer, a number of clinical trials have investigated the effect of modulation of autophagy for the treatment of tumors.…”

Section: Targeting Glutaminolysis and Autophagy As An Anticancer Therapymentioning

confidence: 99%

Glutaminolysis and autophagy in cancer

et al. 2015

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“…Since the 1990s, studies have highlighted the occurrence of autophagy in AL cells. Reviewing the ambiguous importance of autophagy in either promoting or suppressing AL cell growth and survival, Evangelisti et al (4) indicated that autophagy may represent a distinct mechanism of cell death, referred to as autophagic cell death (ACD), which also occurs in established tumors, including AL (5)(6)(7)(8). In addition, autophagy can promote necroptosis, a non-apoptotic form of regulated cell death (9)(10).…”

Section: Introductionmentioning

confidence: 99%

Role of caspase-10 in the death of acute leukemia cells

et al. 2016

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Abstract. Autophagy can protect cells from stress, but can also induce cancer cell death. Caspase-10 is now considered to be a factor that is associated with autophagy in cancer. The present study therefore investigated whether caspase-10 affects autophagy in acute leukemia cells. The rates of survival vs. apoptosis in acute leukemia HL-60 and Jurkat cells treated with drugs were tested using cell viability assays and flow cytometry, and the levels of caspase-3 and -10 were tested by western blotting. In HL-60 cells that were treated with chemotherapy drugs combined with a caspase-10 inhibitor, the rate of survival decreased significantly compared with HL-60 cells treated with chemotherapy drugs alone. In contrast, the rate of survival of Jurkat cells treated with chemotherapy drugs combined with the caspase-10 inhibitor increased significantly compared with Jurkat cells treated with chemotherapy drugs alone. The results of the flow cytometry and western blotting showed that the changes in the survival rate may be caused by a change in the amount of apoptosis occurring in the Jurkat cells treated with chemotherapy drugs combined with the caspase-10 inhibitor. However, in HL-60 cells undergoing this combination treatment, the change in the survival rate was not caused by a change in the rate of apoptosis. When HL-60 cells were treated with the chemotherapy drugs combined with the caspase-10 inhibitor and the autophagy inhibitor 3-methyl adenine, the survival rate increased, whereas the rate of apoptosis did not change. These results show that caspase-10 may be associated with autophagy in acute myeloid leukemia cells, but not in acute lymphatic leukemia cells.

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Autophagy in tumour cell death

Cited by 110 publications

References 98 publications

Small Molecule Inhibition of MDM2–p53 Interaction Augments Radiation Response in Human Tumors

Small Molecule Inhibition of MDM2–p53 Interaction Augments Radiation Response in Human Tumors

Glutaminolysis and autophagy in cancer

Role of caspase-10 in the death of acute leukemia cells

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