Anti-proliferative activity of biochanin A in human osteosarcoma cells via mitochondrial-involved apoptosis

Hsu, Yen-Nien; Shyu, Huey-Wen; Hu, Tsui-Wen; Yeh, Jou-Pei; Lin, Ya-Wen; Lee, Ling-Yi; Yeh, Yao‐Tsung; Dai, Hongying; Perng, Daw‐Shyong; Su, Shih Bin; Huang, Yu‐Hsuan; Su, Shu-Jem

doi:10.1016/j.fct.2017.12.062

Cited by 52 publications

(40 citation statements)

References 52 publications

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“…In general, two major signaling pathways control apoptosis: (i) mitochondria-mediated or intrinsic pathway and (ii) death receptor-mediated or extrinsic pathway [45]. When the cell undergoes pro-apoptotic stimuli, such as deprivation of growth factors, DNA damage, hypoxia, activation of oncogenes, among others, the signals that are translated converge mainly to mitochondria causing the collapse of the potential of the internal mitochondrial membrane (∆ψm) that trigger death by apoptosis [46]. The results obtained in this test demonstrated that the compounds elicited pro-apoptotic effects that induced mitochondrial depolarization in HL-60 cells.…”

Section: Evaluation Of Mitochondrial Transmembrane Potential (∆ψM)mentioning

confidence: 99%

Biological Evaluation of Arylsemicarbazone Derivatives as Potential Anticancer Agents

et al. 2019

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Fourteen arylsemicarbazone derivatives were synthesized and evaluated in order to find agents with potential anticancer activity. Cytotoxic screening was performed against K562, HL-60, MOLT-4, HEp-2, NCI-H292, HT-29 and MCF-7 tumor cell lines. Compounds 3c and 4a were active against the tested cancer cell lines, being more cytotoxic for the HL-60 cell line with IC50 values of 13.08 μM and 11.38 μM, respectively. Regarding the protein kinase inhibition assay, 3c inhibited seven different kinases and 4a strongly inhibited the CK1δ/ε kinase. The studied kinases are involved in several cellular functions such as proliferation, migration, cell death and cell cycle progression. Additional analysis by flow cytometry revealed that 3c and 4a caused depolarization of the mitochondrial membrane, suggesting apoptosis mediated by the intrinsic pathway. Compound 3c induced arrest in G1 phase of the cell cycle on HL-60 cells, and in the annexin V assay approximately 50% of cells were in apoptosis at the highest concentration tested (26 μM). Compound 4a inhibited cell cycle by accumulation of abnormal postmitotic cells at G1 phase and induced DNA fragmentation at the highest concentration (22 μM).

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Section: Evaluation Of Mitochondrial Transmembrane Potential (∆ψM)mentioning

confidence: 99%

Biological Evaluation of Arylsemicarbazone Derivatives as Potential Anticancer Agents

et al. 2019

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“…The MAPK family has extracellular signal-regulated kinases (ERK), p38 MAPK, and JNK [73]. While ERK1/2 predominantly operates cell proliferation, JNK and p38 participate in cell death pathways.…”

Section: Apoptotic Cell Death Induced By Doxorubicinmentioning

confidence: 99%

“…Both pathways have a role in the trigger of apoptosis as upstream (initiator) caspase, e.g., caspase-8 and -9, and downstream (effector) caspase, e.g., caspase-3, -6 and -7 [76]. When MMP is depolarized and opened, mitochondrial apoptotic factors are released such as cytochrome-c and AIF to the cytosol [73]. Cytochrome-c can contain an apoptosome formation with APAF-1, caspase-9.…”

Section: Apoptotic Cell Death Induced By Doxorubicinmentioning

confidence: 99%

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Mitochondrial Dysfunction Associated with Doxorubicin

Güven¹,

Sevgiler²,

Taşkın³

2018

Mitochondrial Diseases

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Cancer prevalence is scaling up each year. Anthracycline groups are still the best chemotherapeutic agent. The most popular anticancer drug in the group is doxorubicin (DOX). Unfortunately, DOX has potent toxicity on noncancerous tissues, e.g., heart, kidneys, etc. However, it is well documented that the severest toxicity of the drug affects heart tissue. Of course, some reasons have been suggested why and/or how the heart is so vulnerable to toxicity. The primary mechanism responsible for DOX's cardiospecific toxicity remains unidentified so far; however, mitochondrial dysfunction induced by DOX is now considered one of the leading reasons for DOX's toxicities and undesired side effects. Mitochondrial reactive oxygen production in the heart is a significant contributor to developing mitochondrial dysfunction-exposed DOX based on a variety of evidence. The objective of this review chapter is to critically evaluate and highlight the role of mitochondria in the development of DOX-induced cardiotoxicity. TurkeyMitochondrial Dysfunction Associated with Doxorubicin http://dx.doi.org/10.5772/intechopen.80284 353

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“…Unfortunately, the clinical use of this drug is hampered due to the cumulative dose‐related cardiotoxicity and vascular damage, which may ultimately lead to a severe and irreversible form of vascular injury and cytotoxicity (Ohlig et al, ). Although numerous underlying mechanisms have been proposed, most studies support the view that an increase in oxidative stress, can be evidenced by increases in the levels of reactive oxygen species (ROS; Zhao et al, ), and lipid peroxidation (Benzer, Kandemir, Ozkaraca, Kucukler, & Caglayan, ), along with reductions in the levels of the antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], glutathione), mitochondrial membrane potential (MMP) and sulfhydryl groups (Hsu et al, ; Magalhães et al, ), in the pathogenesis of DOX‐induced vascular injury and cytotoxicity. This suggests that reductions in the levels of diverse antioxidant enzymes represent a common response to DOX treatment (Li, Danelisen, & Singal, ).…”

Section: Introductionmentioning

confidence: 99%

Protective effects of S‐carvedilol on doxorubicin‐induced damages to human umbilical vein endothelial cells and rats

Lan

et al. 2019

J of Applied Toxicology

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Doxorubicin (DOX) is a highly active anticancer drug with severe cytotoxicity, which is strongly associated with oxidative stress. Carvedilol (CAR), used as its racemate with S-CAR and R-CAR (1:1), has been previously reported to ameliorate the DOX-induced cytotoxicity. However, the main contributor from CAR of its protective effects has not been clear. Therefore, in this study, we aimed to investigate further the different effects of CAR enantiomers on DOX-induced cytotoxicity in human umbilical vein endothelial cells and rats, respectively. Results indicated that S-CAR could significantly attenuate DOX-induced cell death, apoptotic morphological changes, decrease the mitochondrial membrane potential and oxidative stress responses by increasing the superoxide dismutase and catalase activities, and decreasing malondialdehyde contents and reactive oxygen species levels via the phosphoinositide 3-kinase/AKT/endothelial nitric oxide synthase pathway in vitro.Consistent with the in vitro study, the protective effects of S-CAR on the myocardial tissues and hemodynamics were also detected in rats suffering because of DOX treatment. With the obtained results, we can first conclude that S-CAR provides superior protection to injury induced by DOX relative to that of racemic CAR and R-CAR.

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Anti-proliferative activity of biochanin A in human osteosarcoma cells via mitochondrial-involved apoptosis

Cited by 52 publications

References 52 publications

Biological Evaluation of Arylsemicarbazone Derivatives as Potential Anticancer Agents

Biological Evaluation of Arylsemicarbazone Derivatives as Potential Anticancer Agents

Mitochondrial Dysfunction Associated with Doxorubicin

Protective effects of S‐carvedilol on doxorubicin‐induced damages to human umbilical vein endothelial cells and rats

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