Paclitaxel-induced apoptosis in non–small cell lung cancer cell lines is associated with increased caspase-3 activity

Weigel, Tracey L.; Lotze, Michael T.; Kim, Peter K.; Amoscato, Andrew A.; Luketich, James D.; Odoux, Christine

doi:10.1016/s0022-5223(00)70016-x

Cited by 43 publications

(30 citation statements)

References 17 publications

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“…These results indicate that it may be possible to reduce the side effects of PTX whilst enhancing its clinical efficacy by using it in combination with CZEO. PTX can arrest the cell cycle at the G 2 /M phase and induce caspase-3 enzymatic activity (29)(30)(31)(32). In the present study, treatment with the combination of CZEO and PTX increased the accumulation of cells in the G 2 /M phase, and the expression levels of caspase-3.…”

Section: Discussionsupporting

confidence: 58%

Curcuma zedoaria (Berg.) Rosc. essential oil and paclitaxel synergistically enhance the apoptosis of SKOV3 cells

Zhou

Shen

Xia

et al. 2012

Molecular Medicine Reports

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Abstract. Curcuma zedoaria (Berg.) Rosc. essential oil (CZEO) is the major component of Curcuma zedoaria (Berg.) Rosc., a traditional medicine with antitumor activity. Paclitaxel (PTX) is a first-line chemotherapeutic agent used to treat patients with ovarian cancer. These compounds directly target nuclear DNA, in order to suppress or inhibit tumor cell growth. The present study aimed to determine the synergistic antitumor effects of CZEO and PTX on the SKOV3 human ovarian cancer cell line. SKOV3 cells were treated with CZEO, PTX or a combination of the two and cell viability was detected using cell counting kit-8. In addition, flow cytometry was used to determined cell apoptosis as well as for cell cycle analysis. The morpho logical changes of apoptosis were assessed using Hoechst 33342 staining and the expression levels of apoptotic pathway proteins, including caspase-3 and poly (ADP-ribose) polymerase (PARP), were quantified using western blot analysis. The cell viability assay indicated that either of these compounds alone or in combination suppressed the growth of SKOV3 cells. Furthermore, flow cytometric analysis indicated that treatment with a combination of CZEO and PTX resulted in increased inhibition of proliferation and induction of apoptosis of SKOV3 cells, as compared with treatment with either of the compounds alone. In addition, the protein expression levels of caspase-3 were increased following treatment with a combination of CZEO and PTX. The results of the present study suggested that CZEO and PTX synergistically enhanced the inhibition of SKOV3 proliferation, and the possible underlying mechanism may be the induction of cell apoptosis and cell cycle arrest. This therefore indicated that PTX supplemented with CZEO may be an effective treatment strategy to decrease the dose and toxicity of PTX.

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Section: Discussionsupporting

confidence: 58%

Curcuma zedoaria (Berg.) Rosc. essential oil and paclitaxel synergistically enhance the apoptosis of SKOV3 cells

Zhou

Shen

Xia

et al. 2012

Molecular Medicine Reports

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“…Activation of caspase-3 was also observed during taxol-induced apoptosis in other cell lines including human acute myelocytic leukemia HL-60 cells, 23,27 human lung cancer cell lines 24 and human gastric cell lines. 28,29 These and other results support the notion that different apoptotic pathways may be used by the same apoptotic stimulus in various cells.…”

Section: Caspase-9 Is Not Processed In Taxol-treated Skov3 and Mcf7 Cmentioning

confidence: 81%

“…22 The fact that several apoptotic pathways coexist in mammalian cells suggests that it is important to reveal the mechanism of apoptosis induced by drugs in cancer therapy. Recent studies demonstrated that HL-60 leukemia cell lines 23 and non-small cell lung cancer cell lines 24 are susceptible to taxol-induced apoptosis and that caspase-3 is activated by taxol in these cells. Since breast and ovarian cancer are the main targets of taxol chemotherapy, we decided to study the mechanism of caspase activation following taxol treatment of these types of cancer.…”

Section: Introductionmentioning

confidence: 99%

Taxol-induced apoptosis in human SKOV3 ovarian and MCF7 breast carcinoma cells is caspase-3 and caspase-9 independent

et al. 2002

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Taxol is used in chemotherapy regimens against breast and ovarian cancer. Treatment of tumor model cell lines with taxol induces apoptosis, but exact mechanism is not sufficiently understood. Our results demonstrate that in response to taxol, various cell types differentially utilize distinct apoptotic pathways. Using MCF7 breast carcinoma cells transfected with caspase-3 gene, we showed that taxol-induced apoptosis occurred in the absence of caspase-3 and caspase-9 activation. Similar results were obtained with ovarian SKOV3 carcinoma cells, expressing high level of endogenous caspase-3. In contrast, staurosporine-induced apoptosis in these cells was accompanied by proteolytic cleavage of pro-caspase-3 and induction of caspase-3 enzymatic activity. The effect of taxol appears to be cell type-specific, since taxolinduced apoptosis in leukemia U937 cells involved caspase-3 activation step. We conclude that a unique caspase-3 and caspase-9 independent pathway is elicited by taxol to induce apoptosis in human ovarian and breast cancinoma cells.

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“…32,33 However, data from MCF-7 cells and analysis of caspase-3 knockout mice have shown that caspase-3 deficiency cannot block the caspase cascade. 34 Identification of specific activators of different caspases could be useful for caspase-based gene therapy of cancer.…”

Section: Discussionmentioning

confidence: 99%

Pro-caspase-3 overexpression sensitises ovarian cancer cells to proteasome inhibitors

et al. 2001

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The ubiquitin-proteasome pathway plays a critical role in the degradation of several proteins involved in the cell cycle. Dysregulation of this pathway leads to inhibition of cellular proliferation and the induction of apoptosis. Ubiquitination and its downstream consequences have been investigated intensively as targets for the development of drugs for tumour therapy. Here we have investigated the mechanism of apoptosis induced by the proteasome inhibitors MG-132, lactacystin and calpain inhibitor I (ALLN), in the HEK 293 cell line and the ovarian cancer cell lines SKOV3 and OVCAR3. We have found strong caspase-3-like and caspase-6-like activation upon treatment of HEK 293 cells with MG-132. Using a tricistronic expression vector based on a tetracyclineresponsive system we generated stable SKOV3 nd OVCAR3 cell lines with inducible expression of pro-caspase-3. Induction of pro-caspase-3 expression in normally growing cells does not induce apoptosis. However, in the presence of the proteasome inhibitors MG-132, lactacystin or ALLN we found that cells overexpressing pro-caspase-3 are rapidly targeted for apoptosis. Our results demonstrate that procaspase-3 can sensitise ovarian cancer cells to proteasome inhibitor-induced apoptosis, and a combination of these approaches might be exploited for therapy of ovarian and other cancers.Cell Death and Differentiation (2001) 8, 256 ± 264.

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Paclitaxel-induced apoptosis in non–small cell lung cancer cell lines is associated with increased caspase-3 activity

Cited by 43 publications

References 17 publications

Curcuma zedoaria (Berg.) Rosc. essential oil and paclitaxel synergistically enhance the apoptosis of SKOV3 cells

Curcuma zedoaria (Berg.) Rosc. essential oil and paclitaxel synergistically enhance the apoptosis of SKOV3 cells

Taxol-induced apoptosis in human SKOV3 ovarian and MCF7 breast carcinoma cells is caspase-3 and caspase-9 independent

Pro-caspase-3 overexpression sensitises ovarian cancer cells to proteasome inhibitors

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