Chrysin induces death of prostate cancer cells by inducing ROS and ER stress

Ryu, Soomin; Lim, Whasun; Bazer, Fuller W.; Song, Gwonhwa

doi:10.1002/jcp.25861

Cited by 110 publications

(55 citation statements)

References 42 publications

(49 reference statements)

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“…Previous studies indicate that chrysin reduces cell viability by the activation of cytochrome c and caspase‐3 and ‐9 in human uveal melanoma cells (Xue et al, ). In addition, treatment with chrysin induces abundant ROS generation, leading to lipid peroxidation and alteration of mitochondrial membrane permeabilization in apoptosis of human prostate cancer cells (Ryu et al, ). In accordance with previous researches, chrysin exerted antiproliferative and apoptotic effects on human ovarian cancer cells by inducing ROS production and depolarizing MMP in a dose‐dependent manner.…”

Section: Discussionmentioning

confidence: 99%

“…Chrysin inhibits the growth of lung cancer cells, leading to apoptosis by the activation of caspase-3 and caspase-9, and an increase of the proapoptotic protein, B-cell lymphoma-associated X protein (Bax) (Samarghandian, Nezhad, & Mohammadi, 2014). It stimulates apoptotic events in prostate cancer cells by the accumulation of DNA fragmentation, an increase in the population of cells in the sub-G 1 phase of the cell cycle, and activation of ERK1/2 and p38 proteins (Ryu, Lim, Bazer, & Song, 2017). In addition, chrysin induces cell cycle arrest by reducing cyclin-dependent kinase 2 and 4, and activating p38, leading to the accumulation of p21(Waf1/ Cip1) protein in glioma in vitro (Weng, Ho, & Lin, 2005).…”

Section: Discussionmentioning

confidence: 99%

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Chrysin attenuates progression of ovarian cancer cells by regulating signaling cascades and mitochondrial dysfunction

Lim

Ryu

Bazer

et al. 2017

Journal Cellular Physiology

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Chrysin is mainly found in passion flowers, honey, and propolis acts as a potential therapeutic and preventive agent to inhibit proliferation and invasion of various human cancer cells. Although chrysin has anti-carcinogenic effects in several cancers, little is known about its functional roles in ovarian cancer which shows poor prognosis and chemoresistance to traditional therapeutic agents. In the present study, we investigated functional roles of chrysin in progression of ovarian cancer cells using ES2 and OV90 (clear cell and serous carcinoma, respectively) cell lines. Results of the current study demonstrated that chrysin inhibited ovarian cancer cell proliferation and induced cell death by increasing reactive oxygen species (ROS) production and cytoplasmic Ca levels as well as inducing loss of mitochondrial membrane potential (MMP). Moreover, chrysin activated mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/AKT pathways in ES2 and OV90 cells in concentration-response experiments. Collectively, our results led us to propose that chrysin-induced apoptotic events are mediated by the activation of PI3K and MAPK pathways in human ovarian cancer cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chrysin attenuates progression of ovarian cancer cells by regulating signaling cascades and mitochondrial dysfunction

Lim

Ryu

Bazer

et al. 2017

Journal Cellular Physiology

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“…In detail, the treatment of HCT-116 cell line with 5-hydroxy-7-methoxyflavone led to ROS generation and Ca 2+ release, resulting in ER stress induction. Simultaneously, 5-hydroxy-7-methoxyflavone causes alterations in mitochondrial membrane potential (MMP) and a reduction of the Bcl-2/Bax ratio, leading to activation of caspase-3 and apoptosis progression [32].…”

Section: Flavonoid Derivatives and Phenolic Compoundsmentioning

confidence: 99%

Natural Products Targeting ER Stress, and the Functional Link to Mitochondria

Martucciello

Masullo

Cerulli

et al. 2020

IJMS

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The endoplasmic reticulum (ER) is a dynamic organelle essential for intracellular homeostasis maintenance, controlling synthesis, the folding of secreted and membrane-bound proteins, and transport of Ca2+. During cellular stress, ER dysfunction leads to the activation of unfolded protein response (UPR) due to accumulated misfolded proteins in the ER. This condition is referred as ER stress. Mitochondria and ER form a site of close contact (the mitochondria-associated membrane, MAM) which is a major platform exerting important physiological roles in the regulation of intracellular Ca2+ homeostasis, lipid metabolism, mitochondrial fission, autophagosome formation, and apoptosis progression. Natural products have been receiving increasing attention for their ability to interfere with ER stress. Research works have focused on the capacity of these bioactive compounds to induce apoptosis by activating ER stress through the ER stress-mediated mitochondrial apoptotic pathway. In this review we discuss the role of natural products in the signaling communication between ER and mitochondria, focusing on the effects induced by ER stress including Ca2+ permeability transition and UPR signaling (protein kinase R-like ER kinase/mitofusin 2).

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“…9,10 Recent reports have shown that ER stress is related to apoptosis and the occurrence and progression of tumors. 11,12 Therefore, we speculate that SIL1, as a key regulator of ER function, might have a specific role in tumor development.…”

Section: Introductionmentioning

confidence: 98%

Nucleotide exchange factor SIL1 promotes the progress of breast cancer cells via regulating the cell cycle and apoptosis

et al. 2019

Science Progress

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Breast cancer, as one of the most malignant tumors, poses a serious threat to the lives of females. Nucleotide exchange factor SIL1 is an important regulator of endoplasmic reticulum function that might have a specific role in tumor progression. In this study, we aimed to investigate the effect of SIL1 on the proliferation, apoptosis, and metastasis of human breast cancer. SIL1-specific small interfering RNA was transfected into two breast cancer cell lines, MCF7 and MDA-MB-231, to generate SIL1 knockdown cells. Clone formation and Cell Counting Kit-8 assays were performed to determine cell proliferation. Wound healing and transwell assays were used to detect the cell migration and invasion, respectively. Cell cycle and apoptosis were determined by flow cytometry. The messenger RNA and protein levels of target genes were analyzed using quantitative real-time PCR and western blot. According to the results of TCGA and GTEx database analysis, we determined that SIL1 was overexpressed in 1085 breast cancer samples compared with 291 normal samples. Knockdown of SIL1 inhibited the proliferation, migration, and invasion of MCF7 and MDA-MB-231 cells, accordingly. The cell cycle was blocked at the G1 phase following transfection of SIL1-specific small interfering RNA through the inhibition of Cyclin D1, CDK4, and CDK6. SIL1 knockdown induced apoptosis and also promoted the activity of Caspase9 and Bax. Furthermore, SIL1 was able to promote phosphorylation of ERK1/2. Based on these results, SIL1 might act as an oncogene and accelerate the progression of human breast cancer.

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Chrysin induces death of prostate cancer cells by inducing ROS and ER stress

Cited by 110 publications

References 42 publications

Chrysin attenuates progression of ovarian cancer cells by regulating signaling cascades and mitochondrial dysfunction

Chrysin attenuates progression of ovarian cancer cells by regulating signaling cascades and mitochondrial dysfunction

Natural Products Targeting ER Stress, and the Functional Link to Mitochondria

Nucleotide exchange factor SIL1 promotes the progress of breast cancer cells via regulating the cell cycle and apoptosis

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