Quercetin reverses the doxorubicin resistance of prostate cancer cells by downregulating the expression of c‑met

Xie, Bo; Liang, Zhen; Chen, Jing

doi:10.3892/ol.2017.7561

Cited by 23 publications

(21 citation statements)

References 38 publications

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“…Quercetin may potentiate the effect of fludarabine and ABT-737 against CLL via Mcl-1 inhibition (220), enhance the efficacy of (1) Dox in the Dox resistant prostate cancer (PC)3 cell line (PC3/R) by down-regulating c-met (221) and Dox resistant human leukemic MDR K562/ADR cells by regulating JNK/MAPK (222), (2) TRAIL to pancreatic cancer cells through JNK-mediated cFLIP turnover (223), (3) tamoxifen in tamoxifen-resistant breast cancer cell line (MCF-7Ca/TAM-R) by up-regulating ERα and down-regulating Her-2 (224), etc.…”

Section: Multi-functional Flavonoids Overcome Mdr In Cancermentioning

confidence: 99%

Reversal of Multidrug Resistance in Cancer by Multi-Functional Flavonoids

Shen

et al. 2019

Front. Oncol.

115

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Multidrug resistance (MDR) resulting from different defensive mechanisms in cancer is one of the major obstacles of clinical treatment. To circumvent MDR many reversal agents have been developed, but most of them fail in clinical trials due to severely adverse effects. Recently, certain natural products have been reported to overcome MDR, including flavonoids which are abundant in plants, foods, and herbs. The structure of flavonoids can be abbreviated as C6-C3-C6 (C for carbon), and further categorized into flavonoids, iso-flavonoids and neo-flavonoids, according to their structural backbones. Flavonoids possess multiple bioactivities, and a growing body of research has indicated that both flavonoids and iso-flavonoids can either kill or re-sensitize conventional chemotherapeutics to resistant cancer cells. Here, we summarize the research and discuss the underlying mechanisms, concluding that these flavonoids do not function as specific regulators of target proteins, but rather as multi-functional agents that negatively regulate the key factors contributing to MDR.

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Section: Multi-functional Flavonoids Overcome Mdr In Cancermentioning

confidence: 99%

Reversal of Multidrug Resistance in Cancer by Multi-Functional Flavonoids

Shen

et al. 2019

Front. Oncol.

115

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“…CYP1B1 inhibitors have also been shown to enhance the chemotherapeutic effects of DOX in several cancer cell lines including lung cancer [192][193][194], breast cancer [195][196][197][198][199][200][201], liver cancer [201][202][203][204], glioblastoma [205], prostate cancer [206], colorectal cancer [207,208], gastric cancer [209], and leukemia [210,211]. Importantly, several inhibitors have also been shown to overcome DOX resistance in DOX-resistant cancer cell lines [209,210,[212][213][214][215][216][217].…”

Section: Chemosensitizing Effects Of Cyp1b1 Inhibitorsmentioning

confidence: 99%

“…Protected from chronic DOX in rats [190,229] and mice [185] in vivo. Augmented the cardioprotective effect of losartan against chronic DOX cardiotoxicity [230] Enhanced DOX anti-cancer effects in xenografts of leukemia P388 cells [185], liver cancer cells [231], 4T1 breast cancer cells [232,233] Reversed chemoresistance to DOX in hepatocellular carcinoma cells [202], breast cancer cells [200,212], prostate cancer cells [206], multidrug-resistant leukemia K562 cells [210] Enhanced chemotherapeutic effect of DOX against human breast cancer cells [195][196][197]199,234], human colorectal HT29 cancer cell line [208], neuroblastoma cells [235] Luteolin 79 [219] Protected against DOX-induced cardiomyocyte toxicity in vitro [188] Attenuated acute DOX-induced myocardial lipid peroxidation in vivo [236] Luteolin ( [240] Induced CYP1B1 gene expression [241,242] Protected from chronic DOX-induced cardiotoxicity in vivo [243,244] Protected from DOX-induced senescence in vascular smooth muscle cells [191] Potentiated the cytotoxic effect of DOX in MCF-7, MCF-7/ADR cells, MDA-MB-231 (breast), PC-3 (prostate), H460 (lung), and BxPC-3 (pancreas) cancer cells [213,[245][246][247]] Attenuated DOX-induced cytotoxicity in MCF-7 breast cancer cells in one study [248] Sensitized diffuse large cell lymphoma to CHOP (cyclophosphamide, DOX, vincristine, prednisone) chemotherapy in SCID tumor-bearing mice in vivo [2...…”

Section: Chemosensitizing Effects Of Cyp1b1 Inhibitorsmentioning

confidence: 99%

CYP1B1 as a therapeutic target in cardio-oncology

2020

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Cardiovascular complications have been frequently reported in cancer patients and survivors, mainly because of various cardiotoxic cancer treatments. Despite the known cardiovascular toxic effects of these treatments, they are still clinically used because of their effectiveness as anti-cancer agents. In this review, we discuss the growing body of evidence suggesting that inhibition of the cytochrome P450 1B1 enzyme (CYP1B1) can be a promising therapeutic strategy that has the potential to prevent cancer treatment-induced cardiovascular complications without reducing their anti-cancer effects. CYP1B1 is an extrahepatic enzyme that is expressed in cardiovascular tissues and overexpressed in different types of cancers. A growing body of evidence is demonstrating a detrimental role of CYP1B1 in both cardiovascular diseases and cancer, via perturbed metabolism of endogenous compounds, production of carcinogenic metabolites, DNA adduct formation, and generation of reactive oxygen species (ROS). Several chemotherapeutic agents have been shown to induce CYP1B1 in cardiovascular and cancer cells, possibly via activating the Aryl hydrocarbon Receptor (AhR), ROS generation, and inflammatory cytokines. Induction of CYP1B1 is detrimental in many ways. First, it can induce or exacerbate cancer treatment-induced cardiovascular complications. Second, it may lead to significant chemo/radio-resistance, undermining both the safety and effectiveness of cancer treatments. Therefore, numerous preclinical studies demonstrate that inhibition of CYP1B1 protects against chemotherapy-induced cardiotoxicity and prevents chemo- and radio-resistance. Most of these studies have utilized phytochemicals to inhibit CYP1B1. Since phytochemicals have multiple targets, future studies are needed to discern the specific contribution of CYP1B1 to the cardioprotective and chemo/radio-sensitizing effects of these phytochemicals.

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“…Studies have reported that multiple natural drugs can be used as sensitizers in chemotherapy. For instance, imperatorin, a linear furanocoumarin compound extracted from the root of Angelica dahurica , has been reported to decrease the cisplatin resistance through suppression of MCL-1 [ 35 ]; Quercetin, a flavonoid that widely distributes in plant-based foods, has been found to reverse the resistance of prostate cancer to doxorubicin-based therapy [ 36 ]; Resveratrol, a natural polyphenol compound, has been proved to restore the sensitivity of glioma cells to temozolamide through inhibiting the activation of Wnt signaling pathway [ 37 ]. As one kind of natural drug, osthole has some anti-tumor activity with low toxicity and little side effects.…”

Section: Discussionmentioning

confidence: 99%

Osthole resensitizes CD133+ hepatocellular carcinoma cells to cisplatin treatment via PTEN/AKT pathway

Sun

et al. 2020

Aging

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The population of CD133 positive cancer cells has been reported to be responsible for drug resistance of hepatocellular carcinoma (HCC). However, the potential molecular mechanism by which CD133 + HCC cells develop drug resistance is still unclear. In this study, we found that CD133 + HepG2 and Huh7 cells were resistant to cisplatin treatment, compared to the CD133 - HepG2 and Huh7 cells. However, treatment with osthole, a natural coumarin isolated from umbelliferae plant monomers, was found to resensitize CD133 + HepG2 and Huh7 cells to cisplatin treatment. In the mechanism research, we found that treatment with osthole increased the expression of PTEN. As a result, osthole inhibited the phosphorylation of AKT and Bad to decrease the amount of free Bcl-2 in CD133 + HepG2 and Huh7 cells. Finally, cisplatin-induced mitochondrial apoptosis was expanded. In conclusion, combination treatment with osthole can resensitize CD133 + HCC cells to cisplatin treatment via the PTEN/AKT pathway.

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Quercetin reverses the doxorubicin resistance of prostate cancer cells by downregulating the expression of c‑met

Cited by 23 publications

References 38 publications

Reversal of Multidrug Resistance in Cancer by Multi-Functional Flavonoids

Reversal of Multidrug Resistance in Cancer by Multi-Functional Flavonoids

CYP1B1 as a therapeutic target in cardio-oncology

Osthole resensitizes CD133+ hepatocellular carcinoma cells to cisplatin treatment via PTEN/AKT pathway

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