Time-Dependent Changes in Factors Involved in the Apoptotic Process in Human Ovarian Cancer Cells as a Response to Cisplatin

Kolfschoten, Geertruida M.; Hulscher, T.M.; Schrier, S.Mariette; Houten, Viola M. M. van; Pinedo, H.M.; Boven, Epie

doi:10.1006/gyno.2001.6537

Cited by 26 publications

(18 citation statements)

References 29 publications

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“…While we have not fully worked out the apoptotic pathway of the antisensetreated U87MG cells, caspase 3 has been shown to be activated in both p53-independent and-dependent apoptosis. [36][37][38] The morphological features of the U87MG cells treated with p53 antisense oligos þ cisplatin also indicated that cell death was by apoptosis (7072.16%) (Fig 2(I)A, lower panel). These features were not present in cells treated with random oligos þ cisplatin (1.971.7%, P ¼ 5.11 Â 10…”

Section: Resultsmentioning

confidence: 84%

Sensitizing glioma cells to cisplatin by abrogating the p53 response with antisense oligonucleotides

et al. 2004

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Most gene therapy strategies related to p53 concentrate on the restoration of the activity of mutant p53, as several observations indicate that tumors and cell lines having the mutant gene are resistant to chemotherapy. However, as there is also some evidence to the contrary, we studied the relationship of the p53 status to the cellular response of glioma cells that were exposed to cisplatin. At a concentration of 2.5 mg/ml (which is about half the peak pharmacological blood level reached during chemotherapy), U373MG glioma cells, which had a mutant p53 gene, were more sensitive to the drug as compared to U87MG glioma cells (with normal p53). The U373MG cells responded with apoptosis while U87MG cells responded with a G2-M arrest. In U87MG cells, blocking the p53 response by antisense oligonucleotides also sensitized the cells to 2.5 mg/ml cisplatin, and shifted the cellular response from arrest to caspase 3-mediated apoptosis. A sensitive, p53-independent, mechanism for chemotherapy-induced apoptosis suggests that, in some cases, p53 abrogation by gene therapy or small molecule-based strategies could be a viable therapeutic strategy.

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Section: Resultsmentioning

confidence: 84%

Sensitizing glioma cells to cisplatin by abrogating the p53 response with antisense oligonucleotides

et al. 2004

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“…Interestingly, ZD1839 alone had no effect on caspase 3 activity, but the addition of ZD1839 to cisplatin -5FU led to a marked increase in Figure 6). Recently, caspase 3 activation has been shown to play an important role in cisplatin-induced apoptosis and to precede the morphological changes typical to apoptosis (Kolfschoten et al, 2002). We feel the supra-additive increase in caspase 3 activity in the presence of ZD1839 and cisplatin -5FU is a molecular illustration of the synergistic interaction observed with this drug combination (Magné et al, 2002a).…”

Section: Effects On Apoptosis (Figures 4 -7 and 9)mentioning

confidence: 78%

Molecular mechanisms underlying the interaction between ZD1839 (‘Iressa’) and cisplatin/5-fluorouracil

et al. 2003

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ZD1839 ('Iressa'), an orally active, selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, is currently being investigated in clinical trials as a treatment for cancer. 'Iressa' is a trademark of the AstraZeneca group of companies. We have previously demonstrated a synergistic interaction between ZD1839 and cisplatin/5-fluorouracil (5FU) in CAL33, a human head and neck cancer cell line that markedly expresses EGFR. This study examined the effects of this drug combination on the cell cycle, cell cycle regulators, apoptosis-related factors, EGFR-related signalling and DNA repair in CAL33 cells. The cells were incubated with ZD1839 alone for 48 h, then cisplatin and 5FU were added. Exposure to the drug combination continued for a further 48 h. ZD1839 alone induced accumulation of cells in the G0/G1 phase of the cell cycle at 24 h accompanied by a concomitant increase in p21, p27 and Bax, a significant decrease in Bcl2 and a decrease in Akt phosphorylation. A decrease in DNA-PK was observed at 48 h. ZD1839 alone had no effect on caspase-3 activity, but addition of ZD1839 to cisplatin-5FU led to a significant increase in caspase-3 activity at 96 h. Thus, ZD1839 affects key cellular pathways controlling cell proliferation, apoptosis and DNA repair. These data provide a rationale to support clinical trials combining ZD1839 and cisplatin -5FU and other protocols that combine EGFR-targeting agents with chemotherapy or radiotherapy.

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“…Results showed that the effect was TdT is able to label blunt ends of double stranded DNA break independent of Recent studies have demonstrated that apoptosis involved in cell death induced by chemotherapeutic agents including cisplatin, cytarabine, camptothecin, amsacrine, etoposide and teniposide. 11,12 There is an accumulating evidence that the efficacy of antitumor agents is related to the intrinsic propensity of the target tumor cells to respond to these agents by apoptosis. [13][14][15] Apoptosis, a physiological mode of cell death, is characterized by reduced cell volume, condensed chromatin in the nucleus, formation of internucleosomal DNA fragmentation and loss of membrane integrity, and generation of apoptotic bodies.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic effect of γ-sitosterol from Kejibeling (<em>Strobilanthes crispus</em>) and its mechanism of action towards <em>c-myc</em> gene expression and apoptotic pathway

et al. 2015

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Abstrak Metode: Penelitian in vitro ini menggunakan kultur sel kanker kolon manusia (Caco-2), sel kanker hepar manusia (HepG2), sel kanker payudara tergantung hormon (MCF-7) dan kultur sel normal hepar manusia (Chang Liver). Efek sitotoksik diukur melalui uji MTT melalui penentuan Abstract Background:This study aimed to analyze the cytotoxicity effect of γ-sitosterol isolated from "Kejibeling" (Strobilanthes crispus), a medicinal plant, on several cancer cell lines. The mechanisms of the effects were studied through the expression of cancer-caused gene, c-myc and apoptotic pathways.

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Time-Dependent Changes in Factors Involved in the Apoptotic Process in Human Ovarian Cancer Cells as a Response to Cisplatin

Cited by 26 publications

References 29 publications

Sensitizing glioma cells to cisplatin by abrogating the p53 response with antisense oligonucleotides

Sensitizing glioma cells to cisplatin by abrogating the p53 response with antisense oligonucleotides

Molecular mechanisms underlying the interaction between ZD1839 (‘Iressa’) and cisplatin/5-fluorouracil

Cytotoxic effect of γ-sitosterol from Kejibeling (<em>Strobilanthes crispus</em>) and its mechanism of action towards <em>c-myc</em> gene expression and apoptotic pathway

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