Induction of p53 and drug resistance following treatment with cisplatin or paclitaxel in ovarian cancer cell lines

Metzinger, Daniel S.; Taylor, Douglas D.; Gerçel-Taylor, Çiçek

doi:10.1016/j.canlet.2005.05.016

Cited by 25 publications

(18 citation statements)

References 21 publications

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“…Tubulin-binding agents with simple chemical structures, such as moscatilin, may be easier to synthesize and develop as clinical drugs. Second, cancer cells can develop resistance to many tubulinbinding agents, such as Taxol and vincristine, because these drugs are substrates of P-glycoprotein (25,26). Moscatilin has effective antiproliferative activity in P-glycoprotein-rich NCI/ADR-Res cells indicating that it is not a P-glycoprotein substrate (Fig.…”

Section: Discussionmentioning

confidence: 99%

Moscatilin Induces Apoptosis in Human Colorectal Cancer Cells: A Crucial Role of c-Jun NH2-Terminal Protein Kinase Activation Caused by Tubulin Depolymerization and DNA Damage

Chen

Pan

Guh

et al. 2008

Clinical Cancer Research

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Purpose: To study the effect of moscatilin (purified from the stem of orchid Dendrobrium loddigesii) on the proliferation of human colorectal cancer HCT-116 cells in vitro and in vivo. Experimental Design: The growth inhibition of moscatilin was screened on several human cancer cell lines. The effect of moscatilin on tubulin was detected in vitro. Following moscatilin treatment on HCT-116 cells, c-Jun NH 2 -terminal protein kinase (JNK) and caspase activation was studied by Western blot analysis, and DNA damage was done by Comet assay. Specific JNK inhibitor SP600125 was cotreated to reverse moscatilin-induced apoptosis. Tumor growth inhibition of moscatilin was done on HCT-116 xenograft models. Results: Moscatilin induced a time-dependent arrest of the cell cycle at G 2 -M, with an increase of cells at sub-G 1 . Moscatilininhibited tubulin polymerization, suggesting that it might bind to tubulins. Moscatilin also induced the phosphorylation ofJNK1/2. SP600125 significantly inhibited the activation of caspase-9 and caspase-3 and the subsequent moscatilin-induced apoptosis. The data suggest that JNK activation may contribute to moscatilin-mediated apoptosis signaling. A parallel experiment showed that SP600125 significantly inhibitsTaxol-and vincristine-induced HCT-116 cell apoptosis. This suggests that the JNK activation may be a common mechanism for tubulinbinding agents. Moreover, moscatilin induces DNA damage, phosphorylation of H2AX and p53, and up-regulation of p21. Our HCT-116 xenograft models show the in vivo efficacy of moscatilin. Conclusions: In summary, our results suggest that moscatilin induces apoptosis of colorectal HCT-116 cells via tubulin depolymerization and DNA damage stress and that this leads to the activation of JNK and mitochondria-involved intrinsic apoptosis pathway.

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Section: Discussionmentioning

confidence: 99%

Moscatilin Induces Apoptosis in Human Colorectal Cancer Cells: A Crucial Role of c-Jun NH2-Terminal Protein Kinase Activation Caused by Tubulin Depolymerization and DNA Damage

Chen

Pan

Guh

et al. 2008

Clinical Cancer Research

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“…Some studies show that drug-induced apoptosis is independent of p53, and others indicate that p53 is required (17)(18)(19)43). In addition, p21 has been reported to have a dual role in apoptosis (29 -34).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-520g Confers Drug Resistance by Regulating p21 Expression in Colorectal Cancer

Zhang

Geng

Talmon

et al. 2015

Journal of Biological Chemistry

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Background: MicroRNAs are small non-protein-coding RNAs that inhibit target gene expression. Results: p53 suppresses miR-520g expression, and miR-520g mediates drug resistance through down-regulation of p21 expression. Conclusion:The p53/miR-520g/p21 signaling axis plays an important role in the response of colorectal cancer to chemotherapy. Significance: Our study identifies miR-520g as a potential target against drug resistance in colorectal cancer, especially in patients with mutant p53.

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“…Exogenously, upregulation of mutated death receptors can also occur at the surface of resistant cancer cells. Apart from death receptors, genetic mutation of the p53 genes and overexpression of p53 can also render cancer cells resistant to drugs like paclitaxel and cisplatin [ 39 ].…”

Section: Defective Apoptotic Machineriesmentioning

confidence: 99%

Nanotechnology to Combat Multidrug Resistance in Cancer

Akhter

Amin

Ahmad

et al. 2014

Resistance to Targeted Anti-Cancer Therapeutics

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Multidrug resistance (MDR) in cancer is a prime obstacle toward successful cancer chemotherapy which is the combination of the complicated mechanisms involving abnormal vasculature, localized area of hypoxia, upregulated ABC transporters, aerobic glycolysis, elevated apoptotic threshold, and increased interstitial fl uid pressure. Nanomedicines in targeted cancer chemotherapy hold great promise as an effective approach to prevail over MDR. Extensive research has been conducted to get success in development of Nanomedicines against MDR that introduced many of them as personalized medicine and in different clinical stages. Nanomedicines can be preferentially accumulated in tumor areas by EPR and by active targeting of upregulated processes such as ABC transporters of cancer cells. In this review, we aimed to discuss different nanomedicines that showed promises against MDR in cancer and improved the chemotherapeutic effi cacy in the last decade. Moreover, different cellular and physiological factors that underlie MDR in cancer will also be discussed.

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Induction of p53 and drug resistance following treatment with cisplatin or paclitaxel in ovarian cancer cell lines

Cited by 25 publications

References 21 publications

Moscatilin Induces Apoptosis in Human Colorectal Cancer Cells: A Crucial Role of c-Jun NH2-Terminal Protein Kinase Activation Caused by Tubulin Depolymerization and DNA Damage

Moscatilin Induces Apoptosis in Human Colorectal Cancer Cells: A Crucial Role of c-Jun NH2-Terminal Protein Kinase Activation Caused by Tubulin Depolymerization and DNA Damage

MicroRNA-520g Confers Drug Resistance by Regulating p21 Expression in Colorectal Cancer

Nanotechnology to Combat Multidrug Resistance in Cancer

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