8-bromo-7-methoxychrysin induces apoptosis by regulating Akt/FOXO3a pathway in cisplatin-sensitive and resistant ovarian cancer cells

Ding, Qing; Chen, Yi; Zhang, Qing; Guo, Yunshan; Huang, Zhangcheng; Dai, Liqing; Cao, Sudan

doi:10.3892/mmr.2015.4039

Cited by 10 publications

(9 citation statements)

References 38 publications

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“…This substituent also effectively enhances the biological activity of other molecules. [91][92][93][94] Compared with compound 6d, compound 6c presented lower LC 50 and LC 90 values to kill Ae. aegypti (L3) larvae and had the advantage of not interfering with the growth of the four environmental indicator organisms.…”

Section: Discussionmentioning

confidence: 95%

Larvicidal activity of substituted chalcones against Aedes aegypti (Diptera: Culicidae) and non‐target organisms

Targanski

Sousa

Pádua

et al. 2020

Pest Management Science

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BACKGROUND: The expansion of Aedes aegypti (Diptera: Culicidae) population has increased the number of cases of arboviruses, in part due to the inefficiency and toxicity of the chemical control methods available to control this vector. We synthesized 19 chalcone derivatives and examined their activity against Ae. aegypti larvae in order to select larvicidal compounds that are non-toxic to other organisms. RESULTS: Seven chalcone derivatives (3a, 3e, 3f, 6a, 6c, 6d, and 6f) had lethal concentrations of substituted chalcones capable of killing 50% (LC 50) values lower than 100 mg mL −1 at 24 h post-treatment, which is the dose that the World Health Organization recommends for the selection of promising larvicides. The type of substituent added to (E)-1,3-diphenylprop-2-en-1-one (3a) markedly affected the larvicidal activity. Addition of chlorine, bromine and methoxy groups to the aromatic rings reduced the larvicidal activity, while replacement of the Bring (phenyl) by a furan ring significantly increased the larvicidal activity. The furan-chalcone (E)-3-(4-bromophenyl)-1-(furan-2-yl)prop-2-en-1-one (6c) killed Ae. aegypti larvae (LC 50 = 6.66 mg mL −1 ; LC 90 = 9.97 mg mL −1) more effectively than the non-substituted chalcone (3a) (LC 50 = 14.43 mg mL −1 ; LC 90 = 20.96 mg mL −1), and was not toxic to the insect Galleria mellonella, to the protozoan Tetrahymena pyriformis, and to the algae Chorella vulgaris. CONCLUSIONS: The substitution pattern of chalcones influenced their larvicidal activity. In the set of compounds tested, (E)-3-(4-bromophenyl)-1-(furan-2-yl)prop-2-en-1-one (6c) was the most effective larvicide against Ae. aegypti, with no clear signs of toxicity to other animal models. Its mechanism of action and effectiveness under field conditions remain to be determined.

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Section: Discussionmentioning

confidence: 95%

Larvicidal activity of substituted chalcones against Aedes aegypti (Diptera: Culicidae) and non‐target organisms

Targanski

Sousa

Pádua

et al. 2020

Pest Management Science

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“…Circumstances have not improved in spite of research efforts and numerous clinical trials aiming to reduce the rates of disability and mortality (3). Thus far, pharmaceutical research has focused on ion channel (Ca 2+ and Na + ) blockers, oxygen free radical scavengers, and excitability and toxicity neurotransmitter blockers (primarily glutamate and glycine receptors) (26). However, the majority of the clinical trials involving such targets have failed due to low efficacy, the number of side effects or study difficulties (26).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-132 modifies angiogenesis in patients with ischemic cerebrovascular disease by suppressing the NF‑κB and VEGF pathway

Che

Zhang

et al. 2017

Mol Med Report

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In the present study, the expression of microRNA (miR)‑132 and the mechanism by which it modifies angiogenesis in patients with ischemic cerebrovascular disease (ICD) was investigated. RNA isolation and reverse transcription‑quantitative polymerase chain reaction were used to measure miR‑132 expression in patients with ICD. Inflammatory factors were measured using ELISA kits and western blotting measured B‑cell lymphoma‑2 (Bcl‑2)‑associated X/Bcl‑2 ratio (Bax/Bcl‑2 ratio), nuclear factor (NF)‑κB p65, matrix metalloproteinase‑9 (MMP‑9), vascular cell adhesion molecule‑1 (VCAM‑1) and protein expression of inducible nitric oxide synthase (iNOS), and vascular endothelial growth factor (VEGF) protein expression. miR‑132 expression in patients with ICD was lower compared with healthy volunteers. PC12 cells were used to create an oxygen glucose deprivation (OGD) model. miR‑132 overexpression in an in vitro model was able to reduce tumor necrosis factor‑a, interleukin (IL)‑1β, IL‑6, IL‑8, cyclooxygenase‑2, caspase‑3 and caspase‑9 levels, suppress Bax/Bcl‑2 ratio, NF‑κB p65, MMP‑9, VCAM‑1, iNOS, VEGF protein expression. The results suggested that miR‑132 may modify angiogenesis in patients with ICD by suppressing the NF‑κB pathway and promoting the VEGF pathway, and may develop into a therapy for ICD in future research.

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“…It is well known that FOXO3a has a crucial role in apoptosis, cell proliferation, DNA damage and resistance to oxidative stress, and thus its deregulation of FOXO3a is highly associated with a series of malignancies [ 60 , 89 – 103 ] (Table 1 ). In most of the malignant cells, the deregulation of FOXO3a is mainly through aberrant PTMs.…”

Section: Foxo3a In Diseases Developmentmentioning

confidence: 99%

“… [ 102 ] Ovarian cancer Inhibition of FOXO3a phosphorylation by BrMC upregulates Bim expression and leads to apoptosis in ovarian cancer cells. [ 103 ] …”

Section: Foxo3a In Diseases Developmentmentioning

confidence: 99%

Critical role of FOXO3a in carcinogenesis

et al. 2018

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FOXO3a is a member of the FOXO subfamily of forkhead transcription factors that mediate a variety of cellular processes including apoptosis, proliferation, cell cycle progression, DNA damage and tumorigenesis. It also responds to several cellular stresses such as UV irradiation and oxidative stress. The function of FOXO3a is regulated by a complex network of processes, including post-transcriptional suppression by microRNAs (miRNAs), post-translational modifications (PTMs) and protein–protein interactions. FOXO3a is widely implicated in a variety of diseases, particularly in malignancy of breast, liver, colon, prostate, bladder, and nasopharyngeal cancers. Emerging evidences indicate that FOXO3a acts as a tumor suppressor in cancer. FOXO3a is frequently inactivated in cancer cell lines by mutation of the FOXO3a gene or cytoplasmic sequestration of FOXO3a protein. And its inactivation is associated with the initiation and progression of cancer. In experimental studies, overexpression of FOXO3a inhibits the proliferation, tumorigenic potential, and invasiveness of cancer cells, while silencing of FOXO3a results in marked attenuation in protection against tumorigenesis. The role of FOXO3a in both normal physiology as well as in cancer development have presented a great challenge to formulating an effective therapeutic strategy for cancer. In this review, we summarize the recent findings and overview of the current understanding of the influence of FOXO3a in cancer development and progression.

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8-bromo-7-methoxychrysin induces apoptosis by regulating Akt/FOXO3a pathway in cisplatin-sensitive and resistant ovarian cancer cells

Cited by 10 publications

References 38 publications

Larvicidal activity of substituted chalcones against Aedes aegypti (Diptera: Culicidae) and non‐target organisms

Larvicidal activity of substituted chalcones against Aedes aegypti (Diptera: Culicidae) and non‐target organisms

MicroRNA-132 modifies angiogenesis in patients with ischemic cerebrovascular disease by suppressing the NF‑κB and VEGF pathway

Critical role of FOXO3a in carcinogenesis

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