2a, a novel curcumin analog, sensitizes cisplatin-resistant A549 cells to cisplatin by inhibiting thioredoxin reductase concomitant oxidative stress damage

Zhou, Binhua P.; Huang, Jianing; Zuo, Yinglin; Li, Baojian; Guo, Qiang; Cui, Baicheng; Shao, Weiwei; Du, Jie; Bu, Xianzhang

doi:10.1016/j.ejphar.2013.03.014

Cited by 27 publications

(21 citation statements)

References 37 publications

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“…We generated CP-resistant A549 cells (A549R) using protocols described previously. 34, 35 These A549R cells displayed upregulated cytoplasmic RAP1 and induced NF- κ B signaling (Figures 6a, b, Supplementary Figure S7b). The tolerance of these cells to CP was well characterized by treating with high dose of CP, which eliminated 60–90% of normal A549 cells within 24 h (Supplementary Figure S7a).…”

Section: Resultsmentioning

confidence: 99%

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Cytoplasmic RAP1 mediates cisplatin resistance of non-small cell lung cancer

et al. 2017

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Cytotoxic chemotherapy agents (e.g., cisplatin) are the first-line drugs to treat non-small cell lung cancer (NSCLC) but NSCLC develops resistance to the agent, limiting therapeutic efficacy. Despite many approaches to identifying the underlying mechanism for cisplatin resistance, there remains a lack of effective targets in the population that resist cisplatin treatment. In this study, we sought to investigate the role of cytoplasmic RAP1, a previously identified positive regulator of NF-κB signaling, in the development of cisplatin resistance in NSCLC cells. We found that the expression of cytoplasmic RAP1 was significantly higher in high-grade NSCLC tissues than in low-grade NSCLC; compared with a normal pulmonary epithelial cell line, the A549 NSCLC cells exhibited more cytoplasmic RAP1 expression as well as increased NF-κB activity; cisplatin treatment resulted in a further increase of cytoplasmic RAP1 in A549 cells; overexpression of RAP1 desensitized the A549 cells to cisplatin, and conversely, RAP1 depletion in the NSCLC cells reduced their proliferation and increased their sensitivity to cisplatin, indicating that RAP1 is required for cell growth and has a key mediating role in the development of cisplatin resistance in NSCLC cells. The RAP1-mediated cisplatin resistance was associated with the activation of NF-κB signaling and the upregulation of the antiapoptosis factor BCL-2. Intriguingly, in the small portion of RAP1-depleted cells that survived cisplatin treatment, no induction of NF-κB activity and BCL-2 expression was observed. Furthermore, in established cisplatin-resistant A549 cells, RAP1 depletion caused BCL2 depletion, caspase activation and dramatic lethality to the cells. Hence, our results demonstrate that the cytoplasmic RAP1–NF-κB–BCL2 axis represents a key pathway to cisplatin resistance in NSCLC cells, identifying RAP1 as a marker and a potential therapeutic target for cisplatin resistance of NSCLC.

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Section: Resultsmentioning

confidence: 99%

“…34, 35 The human bronchial epithelial cell line 16HBE was a kind gift from Sino-French Hoffman Institute, Guangzhou Medical University, Guangdong, China. All cells were cultured based on the guidance from the manufacturer.…”

Section: Methodsmentioning

confidence: 99%

Cytoplasmic RAP1 mediates cisplatin resistance of non-small cell lung cancer

et al. 2017

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“…Recently, curcumin (Yu et al, 2011;Li et al, 2013;Zhou et al, 2013;Yin et al, 2013) and triptolide (Kim et al, 2010;Liu et al, 2012;Wen et al, 2012) are able to potently inhibit the growth of human cancer cells in vitro and prevents tumor growth in vivo via inhibiting cell proliferation and inducing apoptosis. However, both of curcumin and triptolide possess side effects in high concentration (Banjerdpongchai et al, 2005;Clawson et al, 2010;Antonoff et al, 2010;Li et al, 2010;Borja-Cacho et al, 2010;Shakibaei et al, 2013;Du et al, 2013;Jiang et al, 2013).…”

Section: Combined Effects Of Curcumin and Triptolide On An Ovarian Camentioning

confidence: 99%

Combined Effects of Curcumin and Triptolide on an Ovarian Cancer Cell Line

Cai

Lin²,

Li³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Background: As natural medicines in Asia, curcumin and triptolide extracted from different drug plants have proven to possess anticancer potential and widely used for anti-cancer research. The present study attempted to clarify that curcumin and triptolide synergistically suppress ovarian cancer cell growth in vitro. Methods: To test synergic effects, cell viability and apoptosis were analyzed after curcumin and triptolide combination treatment on ovarian cancer cell lines. Synergistic effects on apoptosis induction were determined by lactate dehydrogenase (LDH) leakage assay, intracellular reactive oxygen species (ROS) assay, mitochondrial membrane potential (MMP) loss assay and flow cytometry analysis. Critical regulators of cell proliferation and apoptosis related were analyzed by qRT-PCR and Western blotting. Results: We showed that the combination of curcumin and triptolide could synergistically inhibit ovarian cancer cell growth, and induce apoptosis, which is accompanied by HSP27 and HSP70, indicating that HSP27 and HSP70 play the important role in the synergic effect. Conclusions: From the result present here, curcumin and triptolide combination with lower concentration have a synergistic anti-tumor effect on ovarian cancer and which will have a good potential in clinical applications.Keywords: Curcumin -triptolide -ovarian cancer cell line -cytotoxicity RESEARCH ARTICLE Combined Effects of Curcumin and Triptolide on an Ovarian Cancer Cell LineYing-Ying Cai*, Wei-Ping Lin, Ai-Ping Li, Jian-Yang Xu Pacak et al., 2012;Hsu et al.,2013;Tan et al., 2013;Huang et al., 2013). Recently, curcumin (Yu et al., 2011;Li et al., 2013;Zhou et al., 2013;Yin et al., 2013) and triptolide (Kim et al., 2010;Liu et al., 2012;Wen et al., 2012) are able to potently inhibit the growth of human cancer cells in vitro and prevents tumor growth in vivo via inhibiting cell proliferation and inducing apoptosis. However, both of curcumin and triptolide possess side effects in high concentration (Banjerdpongchai et al., 2005;Clawson et al., 2010;Antonoff et al., 2010;Li et al., 2010;Borja-Cacho et al., 2010;Shakibaei et al., 2013;Du et al., 2013;Jiang et al., 2013).To decrease the side effects and enhance the efficacy of traditional Chinese medicine (TCM) prescriptions, combinations of different TCM herbs is alternative strategy for cancer therapy. The present study was aimed to analysis the combined effect of curcumin and triptolide on ovarian cancer cell lines in vitro. Materials and Methods Reagents and cell cultureCurcumin was purchased from the Sigma-Aldrich Trading Co, Ltd (Shanghai, China); it was dissolved in DMSO to obtain 1 mM stock solution and kept at -20 °C until use, and then diluted in medium to different concentrations. Triptolide (purity > 99.0%, Institute of Human ovarian cancer OVAR3, SKOV3, HO-8910 and A2780 cell lines were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA). Cells were cultured in Dulbecco's Modified Eagle's medium (DMEM) supplemented with 10 % fetal bovine serum (F...

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“…However, some cell lines (PC9, H1975, H1650) become resistant to targeted drugs such as the tyrosine kinase inhibitors (e.g., erlotinib, gefitinib) and have thus been used to expand the potential utility of curcumin to lung cancers harboring/gaining specific mutations. Cotreatment using standard chemotherapy drugs in combination with curcumin enhanced antitumor efficacy of erlotinib (Yamauchi et al, 2014;Li et al, 2014a), cisplatin (Chanvorachote et al, 2009;Ye et al, 2012;Zhou et al, 2013a), and vinorelbine (Chen et al, 2004) by sensitizing cells to drug-induced apoptosis.…”

Section: Models For Tertiary Lung Cancer Preventionmentioning

confidence: 99%

“…Overwhelmingly, mechanisms of action reported for the antitumor efficacy of curcumin in lung cancer cells are via mitochondrial-mediated cell death elicited by an increase in the Bax:B cell lymphoma-2 ratio or by an increase in intracellular reactive oxygen species (ROS) (Chanvorachote et al, 2009;Pongrakhananon et al, 2010;Saha et al, 2010;Wu et al, 2010;Wang et al, 2011Wang et al, , 2013bSahoo et al, 2012;Yang et al, 2012a,b;Liu et al, 2013;Xiao et al, 2013;Chen et al, 2014). Migration and invasive capacity of lung cancer cells may be further decreased by inhibition of matrix metalloprotease expression, decreased nuclear factor-kB, EGFR, Akt, signal transducer and activator of transcription 3, and Cdc42 signaling (Chen et al, 2004(Chen et al, , 2012Lee et al, 2005;Lin et al, 2009Lin et al, , 2012Puliyappadamba et al, 2010;Kaushik et al, 2012;Liu et al, 2013;Yamauchi et al, 2014;Zhou et al, 2013a;Li et al, 2014b). Although drug resistance in lung cancer is a primary cause for therapeutic failure, very few in vitro models of resistance have been used when investigating the potential of curcumin for tertiary interventional strategies.…”

Section: Models For Tertiary Lung Cancer Preventionmentioning

confidence: 99%

Translating Curcumin to the Clinic for Lung Cancer Prevention: Evaluation of the Preclinical Evidence for Its Utility in Primary, Secondary, and Tertiary Prevention Strategies

Howells

Mahale

Sale

et al. 2014

J Pharmacol Exp Ther

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Lung cancer is responsible for over one million deaths worldwide each year. Smoking cessation for lung cancer prevention remains key, but it is increasingly acknowledged that prevention strategies also need to focus on high-risk groups, including ex-smokers, and patients who have undergone resection of a primary tumor. Models for chemoprevention of lung cancer often present conflicting results, making rational design of lung cancer chemoprevention trials challenging. There has been much focus on use of dietary bioactive compounds in lung cancer prevention strategies, primarily due to their favorable toxicity profile and long history of use within the human populace. One such compound is curcumin, derived from the spice turmeric. This review summarizes and stratifies preclinical evidence for chemopreventive efficacy of curcumin in models of lung cancer, and adjudges the weight of evidence for use of curcumin in lung cancer chemoprevention strategies.

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2a, a novel curcumin analog, sensitizes cisplatin-resistant A549 cells to cisplatin by inhibiting thioredoxin reductase concomitant oxidative stress damage

Cited by 27 publications

References 37 publications

Cytoplasmic RAP1 mediates cisplatin resistance of non-small cell lung cancer

Cytoplasmic RAP1 mediates cisplatin resistance of non-small cell lung cancer

Combined Effects of Curcumin and Triptolide on an Ovarian Cancer Cell Line

Translating Curcumin to the Clinic for Lung Cancer Prevention: Evaluation of the Preclinical Evidence for Its Utility in Primary, Secondary, and Tertiary Prevention Strategies

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