Protective role of ABCG2 against oxidative stress in colorectal cancer and its potential underlying mechanism

Nie, Shuang; Huang, Yaqing; Shi, Mengyue; Qian, Xuetian; Li, Hongzhen; Peng, Chunyan; Kong, Bo; Zou, Xiaoping; Shen, Shanshan

doi:10.3892/or.2018.6594

Cited by 14 publications

(10 citation statements)

References 28 publications

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“…Intensive researches have been made over the past decades to give insight into the relationship between reactive oxygen species (ROS) and CRC ( 158 – 160 ). Consistently, Zinkzuk et al in 2019 carried out a study and showed superoxide dismutase was amplified, whereas the activities of catalase, glutathione peroxidase, and glutathione reductase were lower in 50 CRC patients.…”

Section: Clinical Studiesmentioning

confidence: 99%

Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development

et al. 2020

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Receptor for advanced glycation end-products (RAGE) is a multiligand binding and single-pass transmembrane protein taken in diverse chronic inflammatory conditions. RAGE behaves as a pattern recognition receptor, which binds and is engaged in the cellular response to a variety of damage-associated molecular pattern molecules, as well as HMGB1, S100 proteins, and AGEs (advanced glycation end-products). The RAGE activation turns out to a formation of numerous intracellular signaling mechanisms, resulting in the progression and prolongation of colorectal carcinoma (CRC). The RAGE expression correlates well with the survival of colon cancer cells. RAGE is involved in the tumorigenesis, which increases and develops well in the stressed tumor microenvironment. In this review, we summarized downstream signaling cascade activated by the multiligand activation of RAGE, as well as RAGE ligands and their sources, clinical studies, and tumor markers related to RAGE particularly in the inflammatory tumor microenvironment in CRC. Furthermore, the role of RAGE signaling pathway in CRC patients with diabetic mellitus is investigated. RAGE has been reported to drive assorted signaling pathways, including activator protein 1, nuclear factor-κB, signal transducer and activator of transcription 3, SMAD family member 4 (Smad4), mitogen-activated protein kinases, mammalian target of rapamycin, phosphoinositide 3-kinases, reticular activating system, Wnt/β-catenin pathway, and Glycogen synthase kinase 3β, and even microRNAs.

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Section: Clinical Studiesmentioning

confidence: 99%

Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development

et al. 2020

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“…The association between ABCG2 and tumor characteristics has also been widely reported in various cancer types. ABCG2 was positively correlated with the abnormal activation of NF-κB in breast cancer (41) and matrix metalloproteinase 9 in glioma stem cells (42), but played a protective role against oxidative stress and inflammatory factors in colorectal cancer (43). It was of note that the relationship between the Wnt family and ABC family has been explored (44)(45)(46)(47)(48)(49).…”

Section: Discussionmentioning

confidence: 99%

sATP‑binding cassette subfamily�G member�2 enhances the multidrug resistance properties of human nasal natural killer/T�cell lymphoma side population cells

Zhang

Meng

et al. 2020

Oncol Rep

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Extranodal natural killer (NK)/T cell lymphoma, nasal type (ENKL) is a rare type of non-Hodgkin's lymphoma that is associated with limited effective treatment options and unfavorable survival rate, which is partly the result of multidrug resistance (MDR). The presence of side population (SP) cells-SNK-6/ADM-SP (SSP) cells has been previously used to explore mechanisms of drug resistance. ATP-binding cassette subfamily G member 2 (ABCG2) is a gene involved in MDR and is closely associated with SPs. However, the function of ABCG2 in SSP cells is unclear. The present study verified the high expression of ABCG2 in SSP cells. The IC 50 values of doxorubicin, cytarabine, cisplatin, gemcitabine and l-asparaginase were tested to evaluate drug sensitivity in SSP cells with different levels of ABCG2 expression. ABCG2 was identified as a gene promoting in MDR. ABCG2 upregulated cell proliferation, increased clonogenicity, increased invasive ability and decreased apoptosis, in vivo and in vitro, when cells were treated with gemcitabine. To conclude, ABCG2 enhanced MDR and increased the typical biological characteristics associated with cancer cells in SP cells. With further investigation of the ABCG2 gene could have the potential to reverse MDR in ENKL.

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“…Oxidative stress and inflammation play important roles in malignant CRC, and the high expression of ABCG2 in CRC tissue may be a feedback of overoxidation reaction, associated with poor prognosis. A cell culture study showed that downregulation of ABCG2 can inhibit the production of antioxidants, inducing tumor cell growth [15], suggesting that ABCG2 is a potential therapeutic target of CRC. Excessive expression of CYP3A4 is detected in colon tissue [16].…”

Section: Discussionmentioning

confidence: 99%

Anti-Colorectal Cancer Mechanisms of Formononetin Identified by Network Pharmacological Approach

et al. 2019

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This study is funded by the 2018 Innovation Project of Guangxi Graduate Education (No. YCBZ2018036) Background: The network pharmacological approach was used to identity the anti-colorectal cancer (CRC) targets of formononetin (FN) and the molecular mechanisms of FN against CRC. Material/Methods: A tool of the DisGeNET database was used for collection of CRC-based targets. Other tools of SuperPred, herbal ingredients target (HIT), and SwissTargetPrediction databases were applied in prediction of pharmacological targets of FN against cancer. A protein-protein interaction (PPI) network of FN against CRC was obtained by using a STRING database. All top biological functional processes and signaling pathways of FN against CRC were identified by using Database for Annotation, Visualization and Integrated Discovery (DAVID) software and Omicshare cloud platform. Results: The most key anti-CRC targets of FN were identified as tumor protein p53 (TP53), cytochrome P450 3A4 (CYP3A4), ATP binding cassette subfamily G member 2 (ABCG2), tumor necrosis factor (TNF), epidermal growth factor receptor (EGFR), Erb-B2 receptor tyrosine kinase 2 (ERBB2), and cytochrome P450 1A1 (CYP1A1). In further assays, the treatment of CRC by FN was mainly involved in biological functional processes of reactive oxygen species metabolic process, positive regulation of transcription, DNA-templated, positive regulation of nucleic acid-templated transcription, and positive regulation of RNA metabolic process. anti-CRC by FN of signaling pathways were associated with amyotrophic lateral sclerosis (ALS), allograft rejection, cytokine-cytokine receptor interaction, asthma, mitogen-activated protein kinase (MAPK) signaling pathways, and others. Conclusions: The anti-CRC molecular mechanisms of FN are implicated in suppression of cellular proliferation and regulation of cancer-related metabolic pathways. Interestingly, 8 optimal biological targets may be used as potential molecular markers for predicting and treating CRC.

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Protective role of ABCG2 against oxidative stress in colorectal cancer and its potential underlying mechanism

Cited by 14 publications

References 28 publications

Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development

Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development

sATP‑binding cassette subfamily�G member�2 enhances the multidrug resistance properties of human nasal natural killer/T�cell lymphoma side population cells

Anti-Colorectal Cancer Mechanisms of Formononetin Identified by Network Pharmacological Approach

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