Chrysin loaded nanostructured lipid carriers (NLCs) triggers apoptosis in MCF-7 cancer cells by inhibiting the Nrf2 pathway

Sabzichi, Mehdi; Mohammadian, Jamal; Bazzaz, Roya; Pirouzpanah, Mohammad Bagher; Shaaker, Maghsod; Hamishehkar, Hamed; Chavoshi, Hadi; Salehi, Roya; Samadi, Nasser

doi:10.1016/j.procbio.2017.05.024

Cited by 37 publications

(17 citation statements)

References 44 publications

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“…Identification of specific flavonoids that inhibit the Nrf2/ARE pathway in cancer cells would be interesting for exploring their applications in cancer treatment. Interestingly, three flavones, luteolin, apigenin and chrysin, were found to be effective in inhibiting the Nrf2/ARE pathway in different cancer cell lines [ 60 , 61 , 62 , 63 , 68 , 209 ].…”

Section: Promotion Of Cancer Cell Proliferation By Activation Of Nmentioning

confidence: 99%

“…The inhibitory effect of chrysin on the Nrf2/ARE pathway in several cancer cells has been shown. Chrysin reduces the mRNA expression of Nrf2, MRP1, NQO-1, and HO-1 in breast cancer MCF7 cells [ 209 ]. Chrysin sensitizes MCF7 cells to doxorubicin, and the co-treatment with chrysin and doxorubicin increases the apoptotic MCF7 cell population when compared to chrysin or doxorubicin treatment alone [ 209 ].…”

Section: Promotion Of Cancer Cell Proliferation By Activation Of Nmentioning

confidence: 99%

“…Chrysin reduces the mRNA expression of Nrf2, MRP1, NQO-1, and HO-1 in breast cancer MCF7 cells [ 209 ]. Chrysin sensitizes MCF7 cells to doxorubicin, and the co-treatment with chrysin and doxorubicin increases the apoptotic MCF7 cell population when compared to chrysin or doxorubicin treatment alone [ 209 ]. Similar to apigenin, chrysin downregulates the expression of Nrf2 and phase 2 detoxifying enzymes in doxorubicin-resistant hepatocellular carcinoma BEL-7402/ADM cells [ 63 ].…”

Section: Promotion Of Cancer Cell Proliferation By Activation Of Nmentioning

confidence: 99%

“…Furthermore, the inhibitory effects of apigenin were observed in both cancer (BEL-7402/ADM and MCF7) and non-cancer (HUVEC) cells [ 124 ]. At the same time, chrysin sensitizes MCF7 and BEL-7402/ADM cancer cells to doxorubicin, indicating the potential use of chrysin along with chemotherapy to treat breast cancer and hepatocellular carcinoma after further validation in pre-clinical and clinical studies [ 63 , 209 ]. However, chrysin acts as an inhibitor of Nrf2 in HUVECs, as it downregulates the protective effects of hydrogen.…”

Section: Flavonoids and Nrf2/are: A Friend Or Foementioning

confidence: 99%

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Regulation of Nrf2/ARE Pathway by Dietary Flavonoids: A Friend or Foe for Cancer Management?

et al. 2020

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The nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway is an important cell signaling mechanism in maintaining redox homeostasis in humans. The role of dietary flavonoids in activating Nrf2/ARE in relation to cancer chemoprevention or cancer promotion is not well established. Here we summarize the dual effects of flavonoids in cancer chemoprevention and cancer promotion with respect to the regulation of the Nrf2/ARE pathway, while underlying the possible cellular mechanisms. Luteolin, apigenin, quercetin, myricetin, rutin, naringenin, epicatechin, and genistein activate the Nrf2/ARE pathway in both normal and cancer cells. The hormetic effect of flavonoids has been observed due to their antioxidant or prooxidant activity, depending on the concentrations. Reported in vitro and in vivo investigations suggest that the activation of the Nrf2/ARE pathway by either endogenous or exogenous stimuli under normal physiological conditions contributes to redox homeostasis, which may provide a mechanism for cancer chemoprevention. However, some flavonoids, such as luteolin, apigenin, myricetin, quercetin, naringenin, epicatechin, genistein, and daidzein, at low concentrations (1.5 to 20 µM) facilitate cancer cell growth and proliferation in vitro. Paradoxically, some flavonoids, including luteolin, apigenin, and chrysin, inhibit the Nrf2/ARE pathway in vitro. Therefore, even though flavonoids play a major role in cancer chemoprevention, due to their possible inducement of cancer cell growth, the effects of dietary flavonoids on cancer pathophysiology in patients or appropriate experimental animal models should be investigated systematically.

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Section: Promotion Of Cancer Cell Proliferation By Activation Of Nmentioning

confidence: 99%

Section: Promotion Of Cancer Cell Proliferation By Activation Of Nmentioning

confidence: 99%

Section: Promotion Of Cancer Cell Proliferation By Activation Of Nmentioning

confidence: 99%

Section: Flavonoids and Nrf2/are: A Friend Or Foementioning

confidence: 99%

See 2 more Smart Citations

Regulation of Nrf2/ARE Pathway by Dietary Flavonoids: A Friend or Foe for Cancer Management?

et al. 2020

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“…The enzymes that catalyze the chrysin metabolism, such as M-PST, P-PST, and UGT1A6, possess a significant affinity for chrysin, suggesting limited oral bioavailability of chrysin [75]. Several studies have demonstrated some novel dosage forms of chrysin, such as micelles, liposomes, and nanoparticles, as carriers to enhance the bioavailability of chrysin [76][77][78]. Chrysin-loaded poly (d, l-lactic-co-glycolic acid) PLGA and polyvinyl alcohol have been effectively developed for targeting cancer cells [79,80].…”

Section: Modified Chrysinmentioning

confidence: 99%

Anti-neoplastic Potential of Flavonoids and Polysaccharide Phytochemicals in Glioblastoma

Atiq

Parhar

2020

Molecules

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Clinically, gliomas are classified into four grades, with grade IV glioblastoma multiforme being the most malignant and deadly, which accounts for 50% of all gliomas. Characteristically, glioblastoma involves the aggressive proliferation of cells and invasion of normal brain tissue, outcomes as poor patient prognosis. With the current standard therapy of glioblastoma; surgical resection and radiotherapy followed by adjuvant chemotherapy with temozolomide, it remains fatal, because of the development of drug resistance, tumor recurrence, and metastasis. Therefore, the need for the effective therapeutic option for glioblastoma remains elusive. Previous studies have demonstrated the chemopreventive role of naturally occurring pharmacological agents through preventing or reversing the initiation phase of carcinogenesis or arresting the cancer progression phase. In this review, we discuss the role of natural phytochemicals in the amelioration of glioblastoma, with the aim to improve therapeutic outcomes, and minimize the adverse side effects to improve patient’s prognosis and enhancing their quality of life.

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Exploring the Potential Mechanism of Costunolide‐Induced MCF‐7 Cells Apoptosis by Multi‐Spectroscopy, Molecular Docking and Cell Experiments

Liú

Zeng

et al. 2021

Chemistry & Biodiversity

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Breast cancer is one of the most common cancer with high morbidity and mortality in women. This study aimed to explore the potential mechanism of costunolide inducing MCF‐7 cells apoptosis by multi‐spectroscopy, molecular docking, and cell experiments. The results manifested that costunolide interacted with calf thymus DNA (ct‐DNA) in a spontaneous manner, and the minor groove as the preferential binding mode. Furthermore, costunolide inhibited cell proliferation and colony formation. Hoechst 33258 staining showed that cell apoptosis induced by costunolide might be related to DNA damage. The apoptosis mechanism relied on regulating the protein expression of Bax, Bcl‐2, p53, Caspase‐3 and the activation of p38MAPK and nuclear factor κB (NF‐κB) pathways. This study will provide some experimental basis and potential therapeutic strategy for breast cancer treatment.

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Chrysin loaded nanostructured lipid carriers (NLCs) triggers apoptosis in MCF-7 cancer cells by inhibiting the Nrf2 pathway

Cited by 37 publications

References 44 publications

Regulation of Nrf2/ARE Pathway by Dietary Flavonoids: A Friend or Foe for Cancer Management?

Regulation of Nrf2/ARE Pathway by Dietary Flavonoids: A Friend or Foe for Cancer Management?

Anti-neoplastic Potential of Flavonoids and Polysaccharide Phytochemicals in Glioblastoma

Exploring the Potential Mechanism of Costunolide‐Induced MCF‐7 Cells Apoptosis by Multi‐Spectroscopy, Molecular Docking and Cell Experiments

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