Adverse drug reactions of anticancer drugs derived from natural sources

Tewari, Devesh; Rawat, Pooja; Singh, Pawan

doi:10.1016/j.fct.2018.11.041

Cited by 74 publications

(34 citation statements)

References 142 publications

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“…Therefore, there is a need to develop more effective and safe treatment options that can minimize these limitations. In this respect, there is increasing attention being paid to the importance of natural compounds derived from herbal medicines and food constituents that have been traditionally used to prevent and treat various diseases [3,4]. In particular, numerous naturally occurring agents have been reported to cause growth arrest and induce apoptosis in cancer cells, without showing toxicity to normal cells [5,6].…”

Section: Introductionmentioning

confidence: 99%

Anti-Proliferative and Pro-Apoptotic Effects of Licochalcone A through ROS-Mediated Cell Cycle Arrest and Apoptosis in Human Bladder Cancer Cells

Hong

Cha

Hwangbo

et al. 2019

IJMS

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Licochalcone A (LCA) is a chalcone that is predominantly found in the root of Glycyrrhiza species, which is widely used as an herbal medicine. Although previous studies have reported that LCA has a wide range of pharmacological effects, evidence for the underlying molecular mechanism of its anti-cancer efficacy is still lacking. In this study, we investigated the anti-proliferative effect of LCA on human bladder cancer cells, and found that LCA induced cell cycle arrest at G2/M phase and apoptotic cell death. Our data showed that LCA inhibited the expression of cyclin A, cyclin B1, and Wee1, but increased the expression of cyclin-dependent kinase (Cdk) inhibitor p21WAF1/CIP1, and increased p21 was bound to Cdc2 and Cdk2. LCA activated caspase-8 and -9, which are involved in the initiation of extrinsic and intrinsic apoptosis pathways, respectively, and also increased caspase-3 activity, a typical effect caspase, subsequently leading to poly (ADP-ribose) polymerase cleavage. Additionally, LCA increased the Bax/Bcl-2 ratio, and reduced the integrity of mitochondria, which contributed to the discharge of cytochrome c from the mitochondria to the cytoplasm. Moreover, LCA enhanced the intracellular levels of reactive oxygen species (ROS); however, the interruption of ROS generation using ROS scavenger led to escape from LCA-mediated G2/M arrest and apoptosis. Collectively, the present data indicate that LCA can inhibit the proliferation of human bladder cancer cells by inducing ROS-dependent G2/M phase arrest and apoptosis.

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Section: Introductionmentioning

confidence: 99%

Anti-Proliferative and Pro-Apoptotic Effects of Licochalcone A through ROS-Mediated Cell Cycle Arrest and Apoptosis in Human Bladder Cancer Cells

Hong

Cha

Hwangbo

et al. 2019

IJMS

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“…Based on an understanding of the signaling mechanisms that regulate the growth of tumor cells over the past decade, effective therapies have been developed for the treatment of cancer patients. However, although various side effects, including limited efficacy and drug resistance, need to be solved, chemotherapy is still the main approach to cancer therapy [1,2,3,4]. Therefore, in order to develop safer and effective therapies that can overcome these problems, there is a growing interest in natural products that can block the proliferation of cancer cells without affecting normal cells [5,6,7,8].…”

Section: Introductionmentioning

confidence: 99%

Induction of G2/M Cell Cycle Arrest and Apoptosis by Genistein in Human Bladder Cancer T24 Cells through Inhibition of the ROS-Dependent PI3k/Akt Signal Transduction Pathway

et al. 2019

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We examined the anti-cancer effect of genistein, a soy-derived isoflavone, in human bladder transitional cell carcinoma T24 cells. According to our data, genistein induced G2/M phase arrest of the cell cycle and apoptosis. Genistein down-regulated the levels of cyclin A and cyclin B1, but up-regulated the levels of p21WAF1/CIP1, cyclin-dependent kinase (Cdk) inhibitor, that was complexed with Cdc2 and Cdk2. Furthermore, genistein induced the activation of caspases (caspase-3, -8 and -9), and cleavage of poly (ADP-ribose) polymerase cleavage. However, genistein-induced apoptosis was significantly inhibited by a pan-caspase inhibitor, indicating that the induction of apoptosis by genestein was caspase-dependent. In addition, genistein increased the cytosolic release of cytochrome c by increasing the Bax/Bcl-2 ratio and destroying mitochondria integrity. Moreover, genistein inactivated the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway, while LY294002, a PI3K/Akt inhibitor, increased the apoptosis-inducing effect of genistein. Genistein further increased the accumulation of reactive oxygen species (ROS), which was significantly suppressed by N-acetyl cysteine (NAC), a ROS scavenger, and in particular, NAC prevented genistein-mediated inactivation of PI3K/Akt signaling, G2/M arrest and apoptosis. Therefore, the present results indicated that genistein promoted apoptosis induction in human bladder cancer T24 cells, which was associated with G2/M phase cell cycle arrest via regulation of ROS-dependent PI3K/Akt signaling pathway.

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“…Stating the hematologic toxicity differs from one case to another and depends on the used agents, the administered dosages, the way of administration; it is also influenced by the therapeutic antecedents (previous cytotoxic chemotherapy, applied therapeutic strategy and the biologic status of the patient) [17][18][19].…”

Section: Resultsmentioning

confidence: 99%

“…Medullary aplasia represents the most dangerous picture which may occur after chemotherapy and its seriousness is given by the possibility for an infectious clinical picture to occur, which may lead to septicemia, to a hemorrhagic syndrome or to mucosal lesions associated with hemorrhage and necrosis [7][8][9][10][11][12][13][14][15][16][17][18][19].…”

Section: Resultsmentioning

confidence: 99%

Considerations on the Hematologic Toxicity of the all IC-BFM 2002/2009 Therapeutic Protocol in Children with Acute Lymphoblastic Leukemia

Singer¹,

Dinescu²,

Tudoraşcu³

et al. 2019

Rev. Chim.

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Acute lymphoblastic leukemia (ALL) is the most frequent malign hematologic disease in children. We studied the hematologic toxicity caused by the cytostatic treatment which was administered to the children diagnosed with ALL, according to the ALL-IC-BFM 2002/2009 protocol. The study included a number of 15 children with ALL who were treated from 2008 to 2018 within the Oncopediatrics Department of the 2nd Pediatric Clinic of the Emergency County Hospital in Craiova. We decided upon the level of toxicity in blood values, taking into account the severity level (G), according to the Common Terminology Criteria for Adverse Events 2010 guideline and we calculated the mean value of the hemoglobin, leukocytes, neutrophils, and thrombocytes in the children with ALL, for every phase of the cytostatic treatment. The most severe toxicity (grade 4 of severity) was registered in neutrophils (7/15 patients), during the induction and re-induction periods; 4 of these patients had severe infections.

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Adverse drug reactions of anticancer drugs derived from natural sources

Cited by 74 publications

References 142 publications

Anti-Proliferative and Pro-Apoptotic Effects of Licochalcone A through ROS-Mediated Cell Cycle Arrest and Apoptosis in Human Bladder Cancer Cells

Anti-Proliferative and Pro-Apoptotic Effects of Licochalcone A through ROS-Mediated Cell Cycle Arrest and Apoptosis in Human Bladder Cancer Cells

Induction of G2/M Cell Cycle Arrest and Apoptosis by Genistein in Human Bladder Cancer T24 Cells through Inhibition of the ROS-Dependent PI3k/Akt Signal Transduction Pathway

Considerations on the Hematologic Toxicity of the all IC-BFM 2002/2009 Therapeutic Protocol in Children with Acute Lymphoblastic Leukemia

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