Disease relevance of C08545

• The cytotoxic activity of the glycosyl derivatives was investigated and compared with that of squamocin and dihydrosquamocin against human epidermoid carcinoma cells (KB), African green monkey (Cercopithecus aethiops) kidney epithelial cells (VERO), and mouse lymphocytic leukemia cells (L1210) [1].
• Antitumoral effects of squamocin on parental and multidrug resistant MCF7 (human breast adenocarcinoma) cell lines [2].
• Induction of G2/M phase arrest by squamocin in chronic myeloid leukemia (K562) cells [3].

High impact information on C08545

• Several glycosyl derivatives of squamocin (1) have been synthesized by glycosylation under Lewis acid catalysis with two different 1-O-acetyl sugars [1].
• These findings provide the evidence that squamocin can activate IK(Ca) in coronary arterial smooth muscle cells [4].
• The patch-clamp recording technique was used to investigate the effect of squamocin, an Annonaceous acetogenin, on ion currents in cultured smooth muscle cells of human coronary artery [4].
• Initial transient activation of IK(Ca) may reflect the squamocin-induced Ca2+ release from intracellular Ca2+ stores, whereas the sustained activation of IK(Ca) may arise from the squamocin-induced Ca2+ influx across the cell membrane [4].
• The stimulatory effect of squamocin on these channels should affect the functional activity of vascular smooth muscle cells [4].

Biological context of C08545

• Involvement of caspase-3 activation in squamocin-induced apoptosis in leukemia cell line HL-60 [5].
• Squamocin inhibited proliferation of both cell lines identically, by blocking the cell cycle in the G1-phase [2].
• Semisynthesis of heterocyclic analogues of squamocin, a cytotoxic annonaceous acetogenin, by an unusual oxidative decarboxylation reaction [6].
• Our results from this study showed that squamocin inhibited proliferation of HL-60 cells with IC50 value of 0.17 microg/ml and induced apoptosis of HL-60 cells [5].
• Pretreatment of HL-60 cells with caspase-3 specific inhibitor DEVD-CHO prevented squamocin-induced DNA fragmentation, PARP cleavage and cell death [5].

Anatomical context of C08545

• Annonaceous acetogenins: the hydroxyl groups and THF rings are crucial structural elements for targeting the mitochondria, demonstration with the synthesis of fluorescent squamocin analogues [7].
• Investigation of the mechanism of squamocin-induced apoptosis revealed that treatment of HL-60 cells with squamocin resulted in extensive nuclear condensation [5].
• Squamocin was found to inhibit the growth of K562 cells in a time- and dose-dependent manner [3].

Associations of C08545 with other chemical compounds

• A novel acetogenin, joolanin ( 1), along with eight known acetogenins, squamocin ( 2), desacetyluvaricin ( 3), chamuvarinin ( 4), tripoxyrollin ( 5), diepoxyrollin ( 6), dieporeticanin-1 ( 7), dieporeticanin-2 ( 8) and dieporeticenin ( 9) were isolated from the seeds of UVARIA CHAMAE (Annonaceae) [8].
• Bioactivity-directed fractionation of the MeOH extract of the stem barks of Rollinia emarginata resulted in the isolation of six compounds, four acetogenins, rolliniastatin-1, sylvaticin, squamocin, and rollidecin B, one lignan, lirioresinol B, and an oxoaporphine, liriodenin [9].
• Cytotoxic activity of adriamycin was not restored in MCF7-R Pgp expressing cells by squamocin addition [2].

Gene context of C08545

• These results suggest that squamocin inhibits the proliferation of K562 cells via G2/M arrest in association with the induction of p21, p27 and the reduction of Cdk1 and Cdc25C kinase activities [3].
• Selective cytotoxicity of squamocin on T24 bladder cancer cells at the S-phase via a Bax-, Bad-, and caspase-3-related pathways [10].
• These results suggest that apoptosis of HL-60 cells induced by squamocin requires caspase-3 activation and is related to SAPK activation [5].

Analytical, diagnostic and therapeutic context of C08545

• The expression levels of protein bcl-2, bax have no change in response to squamocin treatment in HL-60 cells, whereas stress-activated protein kinase (SAPK/JNK) was activated after treatment with squamocin in HL-60 cells [5].

References