Mechanisms of Anticancer Drug Resistance in Hepatoblastoma

Marin, José J.G.; Cives-Losada, Candela; Asensio, Maitane; Lozano, Elisa; Briz, Óscar; Macı́as, Rocı́o I.R.

doi:10.3390/cancers11030407

Cited by 45 publications

(55 citation statements)

References 149 publications

(208 reference statements)

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“…Chemoresistance arises after long-time exposures to anticancer drugs [81,82]. The difference between temporary treatment and continuous treatment leads to different levels of ROS homeostasis in cancer cells.…”

Section: Redox Homeostasis In Tumorigenesismentioning

confidence: 99%

“…The EMT process allows metastatic tumor cells to migrate to organs. Altered intracellular ROS levels may lead to the promotion of EMT in cancer cell lines that are resistant to anti-cancer drugs [81,108]. Several proteins function in the development of chemoresistance in metastatic advanced carcinomas [151,152].…”

Section: Redox-mediated Mechanism Of Chemoresistancementioning

confidence: 99%

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Redox-Mediated Mechanism of Chemoresistance in Cancer Cells

et al. 2019

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Cellular reactive oxygen species (ROS) status is stabilized by a balance of ROS generation and elimination called redox homeostasis. ROS is increased by activation of endoplasmic reticulum stress, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family members and adenosine triphosphate (ATP) synthesis of mitochondria. Increased ROS is detoxified by superoxide dismutase, catalase, and peroxiredoxins. ROS has a role as a secondary messenger in signal transduction. Cancer cells induce fluctuations of redox homeostasis by variation of ROS regulated machinery, leading to increased tumorigenesis and chemoresistance. Redox-mediated mechanisms of chemoresistance include endoplasmic reticulum stress-mediated autophagy, increased cell cycle progression, and increased conversion to metastasis or cancer stem-like cells. This review discusses changes of the redox state in tumorigenesis and redox-mediated mechanisms involved in tolerance to chemotherapeutic drugs in cancer.

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Section: Redox Homeostasis In Tumorigenesismentioning

confidence: 99%

Section: Redox-mediated Mechanism Of Chemoresistancementioning

confidence: 99%

Redox-Mediated Mechanism of Chemoresistance in Cancer Cells

et al. 2019

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“…Most drugs based on the mechanisms of anticancer resistance in HB will act on pathways such as p53, tyrosine kinase, cell cycle control, and transcriptional and translational events. A specific gene,CYP3A4, upregulated in Set-3, is related to five drugs used in the treatment of HBs 44 , particularly etoposide (a drug used in neoadjuvant chemotherapy), which causes demethylation in liver cells 45,46 , and Sorafenib, a kinase inhibitor mainly oxidized by CYP3A4 , with the collaboration ofCYP1A1 and CYP1B1 47 . Vincristine, Cyclophosphamide and Isofosfamide are also metabolized by CYP3A4 [48][49][50][51] .…”

Section: Discussionmentioning

confidence: 99%

Dna Methylation as a Key Epigenetics Player for Hepatoblastoma Stratification

Rivas¹,

Aguiar²,

Fernandes³

et al. 2020

Preprint

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Background: Hepatoblastoma (HB) is a rare embryonal liver tumor occurring in the pediatric population, and although intrinsic biological differences between tumors can impact HBs prognosis, few groups have studied this aspect. Given the crescent relevance of epigenetic mechanisms in the genesis and progression of these tumors, we aim to classify HB samples according to the different stages of liver development as well as DNA methylation machinery. Procedures: Using bioinformatics tools, we evaluate the expression of 24 genes associated with epigenetics and stages of hepatocyte differentiation as well as global DNA methylation to propose a stratification model for HB. Results: Based on the gene expression profiles of DNA methylation machinery and hepatocyte differentiation markers, HBs were clustered into three groups. Besides reinforcing the molecular heterogeneity of these embryonal tumors, our data propose that a panel of 13 genes can be used for HB stratification (TET1,

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“…In HB patients, the high-risk group is characterized by a marked chemoresistance and poor outcome [75]. Multidrug resistance often occurs after four cycles of chemotherapy [12].…”

Section: Nk-1r Antagonists As Anti-hb Drugs: Mechanisms Of Actionmentioning

confidence: 99%

Neurokinin-1 Receptor Antagonists against Hepatoblastoma

Muñoz

Rosso

Coveñas

2019

Cancers

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Hepatoblastoma (HB) is the most common malignant liver tumor that occurs during childhood. The prognosis of children with HB is favorable when a complete surgical resection of the tumor is possible, but for high-risk patients, the prognosis is much worse. New anti-HB strategies must be urgently developed. The undecapeptide substance P (SP) after binding to the neurokinin-1 receptor (NK-1R), regulates cancer cell proliferation, exerts an antiapoptotic effect, induces cell migration for invasion/metastasis, and triggers endothelial cell proliferation for neoangiogenesis. HB samples and cell lines overexpress NK-1R (the truncated form) and SP elicits HB cell proliferation. One of these strategies could be the use of non-peptide NK-1R antagonists. These antagonists exert, in a concentration-dependent manner, an antiproliferative action against HB cells (inhibit cell proliferation and induce the death of HB cells by apoptosis). NK-1R antagonists exerted a dual effect in HB: Decreased both tumor volume and angiogenic activity. Thus, the SP/NK-1R system is an important target in the HB treatment and NK-1R antagonists could act as specific drugs against HB cells. In this review, we update and discuss the use of NK-1R antagonists in the treatment of HB.

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Mechanisms of Anticancer Drug Resistance in Hepatoblastoma

Cited by 45 publications

References 149 publications

Redox-Mediated Mechanism of Chemoresistance in Cancer Cells

Redox-Mediated Mechanism of Chemoresistance in Cancer Cells

Dna Methylation as a Key Epigenetics Player for Hepatoblastoma Stratification

Neurokinin-1 Receptor Antagonists against Hepatoblastoma

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