Cytotoxicity of diacetoxyscirpenol is associated with apoptosis by activation of caspase-8 and interruption of cell cycle progression by down-regulation of cdk4 and cyclin B1 in human Jurkat T cells

The apoptosis-inducing activity towards leukemia and lymphoma cells in a cyanobacterial culture collection is not associated with mouse bioassay toxicity

“…To assess the apoptogenic activity in the cyanobacteria, extracts of decreasing polarity were tested against jurkat T-cell lymphoma and IPC-81 rat promyelogenic leukemia cells. The jurkat T-cells are widely used to screen for immunosuppressive agents [5, 14, 21, 34], whereas the IPC-81 cells originate from the BNML rat model, which is used for studying human AML and is known to be a reliable predictor of the potential of anti-leukemic drugs (reviewed by [28]). Unlike normal cells of the myeloid lineage the IPC-81 cells can be grown in conventional medium, have very little spontaneous apoptosis [16, 25], and are sensitive to commonly used anti-leukemic drugs [15].…”

Overexpression of cyclin B1 antagonizes chemotherapeutic-induced apoptosis through PTEN/Akt pathway in human esophageal squamous cell carcinoma cells

“…The mitochondrial release of cytochrome c, which is required for the activation of caspase-9 and caspase-3, is a critical event for chemotherapy-mediated apoptosis. 8,25 To understand the deathsignaling pathway underlying cisplatin-and paclitaxel-mediated apoptosis in ESCC cells, we investigated the activation of caspase-9 and caspase-3 after ESCC cells were treated with cisplatin or paclitaxel. As shown in Figure 3, more cleaved caspase-9 was detected in the KYSE150/pcDNA3.1 cells compared with of cyclin B1 could not directly affect the expression of total AKT and phosphorylated form of Akt (p-Akt).…”

“…Thus, it is necessary to better understand the molecular basis of carcinogenesis and to elucidate the signal transduction pathways regulating cell apoptosis, which will provide the impetus for the development of novel molecularly targeted anticancer therapy. It has been illuminated that many proteins can regulate apoptosis in esophageal cancer, including TRAIL, 5,6 CDKs, 7 caspases, 5,6,8 p53, [9][10][11] survivin, 10 N-cadherin, 12 Aurora-A 13 and so on. Within these contexts, therapeutic strategies, which aim to direct induction of cell apoptosis by regulating these proteins, have attracted a great deal of attention.…”

Esophageal Carcinoma

“…59 Survivin can shuttle between the nucleus and the cytoplasm. 15 Some chemical compounds such as the flavonoid baohuoside-I can inhibit cell growth and down-regulate survivin and cyclin D1 expression in EC via β-catenin-dependent signaling, and it is promising in the treatment of EC. 60 In ESCC, overexpression of survivin reduces the percentage of cell death induced by radiation and predicts poor prognosis following radiotherapy.…”

“…115 The Medical Research Council Adjuvant Gastric Infusional Chemotherapy (MAGIC) trial randomized 503 patients with tumor located in stomach, GE junction, or lower esophagus into the surgery-alone group and perioperative chemotherapy group (three preoperative and three postoperative cycles of epirubicin, cisplatin, and 5-fluorouracil (5-FU)-ECF). infusion on days 1,8,15,22, and 29, with concurrent external beam radiation of 41.4 Gy/23 fractions. 119 According to the above evidence, NCCN guidelines recommend that preoperative chemotherapy be used only for adenocarcinoma located in the distal esophagus or GE junction, with ECF regimen as the first option.…”