Induction of apoptosis by cryptophycin 1, a new antimicrotubule agent

Mooberry, Susan L.; Busquets, Lizette; Tien, Georgia

doi:10.1002/(sici)1097-0215(19971104)73:3<440::aid-ijc20>3.0.co;2-f

Cited by 66 publications

(17 citation statements)

References 21 publications

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“…Recently, various cancer chemotherapeutic agents, which block apoptosis through unusual stabilization of microtubules, simultaneously initiated a cascade of events leading to apoptosis. 8,9 Another study 34 indicated that the toxicity of ND was specific for cells from human but not from mouse and hamster. These data suggest that there is a species-specific cytoskeletal damage response pathway.…”

Section: Combined Treatment With Gf and Nd Is Significant For Applicamentioning

confidence: 99%

“…7 Recently, microtubules have been demonstrated to be the new target of many widely used cancer chemotherapeutic agents including taxanes, paclitaxel, cryptophycins and docitaxel by causing specific loss of normal functions of cellular microtubules. 8,9 According to recent reports, microtubule-stabilizing agents such as paclitaxel and docetaxel 10 and microtubule-disrupting drugs such as vincristine, vinblastine and colchicine have antimitotic and apoptosis-inducing activity. 11 In these studies, human leukemic, breast cancer and prostate cancer cells exposed to paclitaxel expressed a phosphorylated form of Bcl-2 and underwent apoptosis, suggesting that phosphorylation of Bcl-2 may inhibit Bcl-2 function.…”

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confidence: 99%

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Griseofulvin potentiates antitumorigenesis effects of nocodazole through induction of apoptosis and G2/M cell cycle arrest in human colorectal cancer cells

Duh

Jeng

et al. 2000

Intl Journal of Cancer

139

116

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Section: Combined Treatment With Gf and Nd Is Significant For Applicamentioning

confidence: 99%

mentioning

confidence: 99%

Griseofulvin potentiates antitumorigenesis effects of nocodazole through induction of apoptosis and G2/M cell cycle arrest in human colorectal cancer cells

Duh

Jeng

et al. 2000

Intl Journal of Cancer

139

116

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“…Antitumor activity in mice was demonstrated at WSU in 1993, with the complete trial published as an example of our laboratory strategy for drug discovery [3]. The mechanism of cytotoxicity of the series is tubulin interaction, with a disruption of tubulin dynamics, resulting in apoptosis of tumor cells [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Cryptophycins-309, 249 and other cryptophycin analogs: Preclinical efficacy studies with mouse and human tumors

et al. 2005

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Cryptophycins-1 and 52 (epoxides) were discovered to have in-vitro and in-vivo antitumor activity in the early 1990s. The chlorohydrins of these, Cryptophycins-8 and 55 (also discovered in the early 1990s) were markedly more active, but could not be formulated as stable solutions. With no method to adequately stabilize the chlorohydrins at the time, Cryptophycin-52 (LY 355073) entered clinical trials, producing only marginal antitumor activity. Since that time, glycinate esters of the hydroxyl group of the chlorohydrins have been synthesized and found to provide stability. Three of the most active were compared herein. Cryptophycin-309 (C-309) is a glycinate ester of the chlorohydrin Cryptophycin-296. The glycinate derivative provided both chemical stability and improved aqueous solubility. After the examination of 81 different Cryptophycin analogs in tumor bearing animals, C-309 has emerged as superior to all others. The following %T/C and Log Kill (LK) values were obtained from a single course of IV treatment (Q2d x 5) against early staged SC transplantable tumors of mouse and human origin: Mam 17/Adr [a pgp (+) MDR tumor]: 0%T/C, 3.2 LK; Mam 16/C/Adr [a pgp (-) MDR tumor]: 0%T/C, 3.3 LK; Mam 16/C: 0%T/C, 3.8 LK; Colon 26: 0%T/C, 2.2 LK; Colon 51: 0%T/C, 2.4 LK; Pancreatic Ductal Adenocarcinoma 02 (Panc 02): 0%T/C, 2.4 LK; Human Colon HCT15 [a pgp (+) MDR tumor]: 0%T/C, 3.3 LK; Human Colon HCT116: 0%T/C, 4.1 LK. One additional analog, Cryptophycin-249 (C-249, the glycinate of Cryptophycin-8), also emerged with efficacy rivaling or superior to C-309. However, there was sufficient material for only a single C-249 trial in which a 4.0 LK was obtained against the multidrug resistant breast adenocarcinoma Mam-16/C/Adr. C-309 and C-249 are being considered as second-generation clinical candidates.

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“…Therefore, overall these data suggest that vinflunine triggers apop- Vinflunine-induced apoptosis in leukaemic cells A Kruczynski et al totic mechanisms involving caspases-3/7 in these P388 leukaemia cells. Involvement of caspases from the caspase-3-like family, as well as PARP cleavage in drug-induced apoptosis has been demonstrated previously for several other microtubule damaging agents, including cryptophycin (Mooberry et al, 1997), taxol, vinblastine, vincristine (Srivastava et al, 1998) and vinorelbine (Toh et al, 1998). A great deal of evidence implicates JNKs signalling in apoptosis occurring in response to diverse cellular stress stimuli, although it probably has a multifunctional role, varying with the stimulus, the cell type, the duration of enzyme activation, or the specific JNKs isoform(s) involved (Stone and Chambers, 2000).…”

Section: Discussionmentioning

confidence: 52%

Characterization of cell death induced by vinflunine, the most recent Vinca alkaloid in clinical development

et al. 2002

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Vinflunine, the most recent Vinca alkaloid in clinical development, demonstrated superior antitumour activity to other Vincas in preclinical tumour models. This study aimed to define its molecular mechanisms of cell killing in both parental sensitive and vinflunine-resistant P388 leukaemia cells. Vinflunine treatment of these cells resulted in apoptosis characterized by DNA fragmentation and proteolytic cleavage of poly-(ADP-ribose) polymerase. Apoptosis-inducing concentrations of vinflunine caused c-Jun N-terminal kinase 1 stimulation, as well as caspases-3/7 activation. This activation of caspases and the induction of apoptosis could be inhibited by the caspase inhibitor acetyl-Asp-Glu-Val-Asp-aldehyde. Interestingly, the apoptosis signal triggered by vinflunine in these P388 cells was not mediated through Bcl-2 phosphorylation. In addition, when vinflunine resistance was developed in P388 cells, it was associated with resistance to vinflunine-induced apoptosis, as reflected by a loss of capacity to induce DNA fragmentation and PARP degradation, and characterized by increased levels of Bcl-2 and Bfl-1/A1. Therefore, these data indirectly implicate Bcl-2 and Bfl-1/A1 in vinflunine-induced cell death mechanisms.

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Induction of apoptosis by cryptophycin 1, a new antimicrotubule agent

Cited by 66 publications

References 21 publications

Griseofulvin potentiates antitumorigenesis effects of nocodazole through induction of apoptosis and G2/M cell cycle arrest in human colorectal cancer cells

Griseofulvin potentiates antitumorigenesis effects of nocodazole through induction of apoptosis and G2/M cell cycle arrest in human colorectal cancer cells

Cryptophycins-309, 249 and other cryptophycin analogs: Preclinical efficacy studies with mouse and human tumors

Characterization of cell death induced by vinflunine, the most recent Vinca alkaloid in clinical development

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