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Kang KA, Piao MJ, Fernando PDSM, Herath HMUL, Boo HJ, Yoon SP, Hyun JW. Oxidative Stress-Mediated RUNX3 Mislocalization Occurs Via Jun Activation Domain-Binding Protein 1 and Histone Modification. Appl Biochem Biotechnol 2024; 196:8082-8095. [PMID: 38683453 PMCID: PMC11645303 DOI: 10.1007/s12010-024-04944-0] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 04/16/2024] [Indexed: 05/01/2024]
Abstract
Runt domain transcription factor 3 (RUNX3) suppresses many different cancer types and is disabled by mutations, epigenetic repression, or cytoplasmic mislocalization. In this study, we investigated whether oxidative stress is associated with RUNX3 accumulation from the nucleus to the cytoplasm in terms of histone modification. Oxidative stress elevated histone deacetylase (HDAC) level and lowered that of histone acetyltransferase. In addition, oxidative stress decreased the expression of mixed lineage leukemia (MLL), a histone methyltransferase, but increased the expression of euchromatic histone-lysine N-methyltransferase 2 (EHMT2/G9a), which is also a histone methyltransferase. Moreover, oxidative stress-induced RUNX3 phosphorylation, Src activation, and Jun activation domain-binding protein 1 (JAB1) expression were inhibited by knockdown of HDAC and G9a, restoring the nuclear localization of RUNX3 under oxidative stress. Cytoplasmic RUNX3 localization was followed by oxidative stress-induced histone modification, activated Src along with RUNX3 phosphorylation, and induction of JAB1, resulting in RUNX3 inactivation.
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Affiliation(s)
- Kyoung Ah Kang
- Jeju Research Center for Natural Medicine, Jeju National University, Jeju, 63243, Republic of Korea
- Department of Biochemistry, Jeju National University College of Medicine, Jeju, 63243, Republic of Korea
| | - Mei Jing Piao
- Jeju Research Center for Natural Medicine, Jeju National University, Jeju, 63243, Republic of Korea
- Department of Biochemistry, Jeju National University College of Medicine, Jeju, 63243, Republic of Korea
| | - Pincha Devage Sameera Madushan Fernando
- Jeju Research Center for Natural Medicine, Jeju National University, Jeju, 63243, Republic of Korea
- Department of Biochemistry, Jeju National University College of Medicine, Jeju, 63243, Republic of Korea
| | | | - Hye-Jin Boo
- Jeju Research Center for Natural Medicine, Jeju National University, Jeju, 63243, Republic of Korea
| | - Sang Pil Yoon
- Jeju Research Center for Natural Medicine, Jeju National University, Jeju, 63243, Republic of Korea
| | - Jin Won Hyun
- Jeju Research Center for Natural Medicine, Jeju National University, Jeju, 63243, Republic of Korea.
- Department of Biochemistry, Jeju National University College of Medicine, Jeju, 63243, Republic of Korea.
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Guo Y, Gao M, Yao Y, Li J, Chen X, Wang X, Chen Z, Yuan Y, Ma W. Prognostic value of CSN5 in patients with digestive system cancers: a systematic review and meta-analysis. BMC Cancer 2022; 22:812. [PMID: 35870903 PMCID: PMC9308938 DOI: 10.1186/s12885-022-09867-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/04/2021] [Accepted: 07/07/2022] [Indexed: 11/10/2022] Open
Abstract
Abstract
Background
Despite the understanding of the COP9 signalosome subunit 5 (CSN5) in tumor genesis, there is no conclusive evidence on its value to predict the survival and prognosis of digestive system tumor patients. Hence this study aimed to evaluate the impact of CSN5 levels on the survival and clinicopathological parameters of digestive system neoplasm patients.
Methods
First, a comprehensive search was conducted in four databases. We utilized the Hazard Ratio (HR) with a 95% confidence interval (CI) to evaluate the prognostic value of CSN5 for the overall survival (OS) and recurrence-free survival (RFS) of patients. Then, we estimated the connection between CSN5 and the clinicopathological parameters based on the Odds Ratio (OR) with the corresponding 95% CI.
Results
This meta-analysis included 22 studies and 2193 patients diagnosed with digestive system tumors. High expression of CSN5 was correlated to poorer OS (HR = 2.28, 95% CI: 1.71–3.03; p < 0.00001). Additionally, high CSN5 levels were correlated with worse invasion depth (OR = 0.49, 95% CI: 0.25–0.96, p = 0.04), positive lymphatic metastasis (OR = 0.28, 95% CI: 0.16–0.47, p = 0.00001), positive distant metastasis (OR = 0.32, 95% CI: 0.13–0.76, p = 0.01) and poorer differentiation degree (OR = 0.34, 95% CI: 0.19–0.60, p = 0.0003). However, we did not detect a correlation between CSN5 expression and age, gender, tumor stage, tumor size or vascular invasion. Furthermore, no significant publication bias was detected.
Conclusion
This meta-analysis demonstrated that the overexpression of CSN5 level might foresee poorer OS in digestive system cancer patients. Additionally, CSN5 levels might be related to the prognosis of digestive system tumors.
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Maslankova J, Vecurkovska I, Rabajdova M, Katuchova J, Kicka M, Gayova M, Katuch V. Regulation of transforming growth factor-β signaling as a therapeutic approach to treating colorectal cancer. World J Gastroenterol 2022. [PMID: 36156927 DOI: 10.3748/wjg.v28.i33.4744.pmid:36156927;pmcid:pmc9476856] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 05/09/2023] Open
Abstract
According to data from 2020, Slovakia has long been among the top five countries with the highest incidence rate of colorectal cancer (CRC) worldwide, and the rate is continuing to rise every year. In approximately 80% of CRC cases, allelic loss (loss of heterozygosity, LOH) occurs in the long arm of chromosome 18q. The most important genes that can be silenced by 18q LOH or mutations are small mothers against decapentaplegic homolog (SMAD) 2 and SMAD4, which are intracellular mediators of transforming growth factor (TGF)-β superfamily signals. TGF-β plays an important role in the pro-oncogenic processes, including such properties as invasion, epithelial-mesenchymal transition (commonly known as EMT), promotion of angiogenesis, and immunomodulatory effects. Several recent studies have reported that activation of TGF-β signaling is related to drug resistance in CRC. Because the mechanisms of drug resistance are different between patients in different stages of CRC, personalized treatment is more effective. Therefore, knowledge of the activation and inhibition of factors that affect the TGF-β signaling pathway is very important.
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Affiliation(s)
- Jana Maslankova
- Department of Medical and Clinical Biochemistry, Faculty of Medicine, Pavol Jozef Safarik University in Kosice, Kosice 04011, Slovakia
| | - Ivana Vecurkovska
- Department of Medical and Clinical Biochemistry, Faculty of Medicine, Pavol Jozef Safarik University in Kosice, Kosice 04011, Slovakia
| | - Miroslava Rabajdova
- Department of Medical and Clinical Biochemistry, Faculty of Medicine, Pavol Jozef Safarik University in Kosice, Kosice 04011, Slovakia
| | - Jana Katuchova
- First Department of Surgery, Medical Faculty of Safarik University, Kosice 04011, Kosicky kraj, Slovakia.
| | - Milos Kicka
- First Department of Surgery, Medical Faculty of Safarik University, Kosice 04011, Kosicky kraj, Slovakia
| | - Michala Gayova
- Department of Burns and Reconstructive Surgery, Medical Faculty at Safarik University and University Hospital, Kosice 04011, Slovakia
| | - Vladimir Katuch
- Department of Neurosurgery, Medical Faculty at Safarik University and University Hospital, Kosice 04011, Slovakia
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Maslankova J, Vecurkovska I, Rabajdova M, Katuchova J, Kicka M, Gayova M, Katuch V. Regulation of transforming growth factor-β signaling as a therapeutic approach to treating colorectal cancer. World J Gastroenterol 2022; 28:4744-4761. [PMID: 36156927 PMCID: PMC9476856 DOI: 10.3748/wjg.v28.i33.4744] [Citation(s) in RCA: 10] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/12/2022] [Revised: 07/06/2022] [Accepted: 08/16/2022] [Indexed: 02/06/2023] Open
Abstract
According to data from 2020, Slovakia has long been among the top five countries with the highest incidence rate of colorectal cancer (CRC) worldwide, and the rate is continuing to rise every year. In approximately 80% of CRC cases, allelic loss (loss of heterozygosity, LOH) occurs in the long arm of chromosome 18q. The most important genes that can be silenced by 18q LOH or mutations are small mothers against decapentaplegic homolog (SMAD) 2 and SMAD4, which are intracellular mediators of transforming growth factor (TGF)-β superfamily signals. TGF-β plays an important role in the pro-oncogenic processes, including such properties as invasion, epithelial-mesenchymal transition (commonly known as EMT), promotion of angiogenesis, and immunomodulatory effects. Several recent studies have reported that activation of TGF-β signaling is related to drug resistance in CRC. Because the mechanisms of drug resistance are different between patients in different stages of CRC, personalized treatment is more effective. Therefore, knowledge of the activation and inhibition of factors that affect the TGF-β signaling pathway is very important.
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Affiliation(s)
- Jana Maslankova
- Department of Medical and Clinical Biochemistry, Faculty of Medicine, Pavol Jozef Safarik University in Kosice, Kosice 04011, Slovakia
| | - Ivana Vecurkovska
- Department of Medical and Clinical Biochemistry, Faculty of Medicine, Pavol Jozef Safarik University in Kosice, Kosice 04011, Slovakia
| | - Miroslava Rabajdova
- Department of Medical and Clinical Biochemistry, Faculty of Medicine, Pavol Jozef Safarik University in Kosice, Kosice 04011, Slovakia
| | - Jana Katuchova
- First Department of Surgery, Medical Faculty of Safarik University, Kosice 04011, Kosicky kraj, Slovakia
| | - Milos Kicka
- First Department of Surgery, Medical Faculty of Safarik University, Kosice 04011, Kosicky kraj, Slovakia
| | - Michala Gayova
- Department of Burns and Reconstructive Surgery, Medical Faculty at Safarik University and University Hospital, Kosice 04011, Slovakia
| | - Vladimir Katuch
- Department of Neurosurgery, Medical Faculty at Safarik University and University Hospital, Kosice 04011, Slovakia
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Mamidi MK, Samsa WE, Danielpour D, Chan R, Zhou G. The transcription co-factor JAB1/COPS5, serves as a potential oncogenic hub of human chondrosarcoma cells in vitro. Am J Cancer Res 2021; 11:5063-5075. [PMID: 34765312 PMCID: PMC8569363] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/11/2019] [Accepted: 06/07/2021] [Indexed: 06/13/2023] Open
Abstract
Chondrosarcoma (CS) is the second most common skeletal malignancy in humans. High-grade CS is aggressive and extremely resistant to chemo- and radio-therapies. The lack of effective treatment options warrants the development of novel therapies. The evolutionarily conserved transcriptional co-factor JAB1 (also known as COPS5/CSN5) has emerged as a novel regulator of tumorigenesis. JAB1 overexpression occurs in many common cancers and is associated with poor prognosis. However, the role of JAB1 in CS pathogenesis was completely unknown. To study JAB1's function in CS, we performed shRNA knockdown (KD) of JAB1 in two high-grade human CS cell lines, SW1353 and Hs819.T, and observed significantly decreased proliferation and colony formations, and increased apoptosis in both CS cell lines upon JAB1-KD. Interestingly, we found that endogenous JAB1 interacted with endogenous SOX9, a potent oncogene and a master regulator of skeletogenesis, in chondrosarcoma cells, but not in primary chondrocytes. JAB1 also binds to the same SOX9-mediated chondrocyte-specific enhancer elements in CS cells. Furthermore, we found that a recently developed, novel, potent, and JAB1-specific small molecule inhibitor, CSN5i-3, can significantly increase apoptosis, drastically alter the activities of several signaling pathways, and modulates the expression of specific Cullin-ring-ligases (CRLs) in CS cells. Finally, our RNA-sequencing analysis in JAB1-KD CS cells identified a total of 2945 differentially expressed genes. Gene set enrichment analysis revealed that JAB1 regulates several essential pathways such as DNA damage response and cell cycle regulation. In conclusion, our study showed that JAB1 might regulate a distinct pro-tumorigenic regulatory network to promote chondrosarcoma pathogenesis.
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Affiliation(s)
- Murali K Mamidi
- Department of Orthopaedics, Case Western Reserve University, Biomedical Research Building#328, 2109 Adelbert Road, Cleveland, OH 44106, USA
- Case Comprehensive Cancer Cancer, Case Western Reserve University, Biomedical Research Building#328, 2109 Adelbert Road, Cleveland, OH 44106, USA
- Stephenson Cancer Center, University of Oklahoma Health Sciences CenterOklahoma, USA
| | - William E Samsa
- Department of Orthopaedics, Case Western Reserve University, Biomedical Research Building#328, 2109 Adelbert Road, Cleveland, OH 44106, USA
- Case Comprehensive Cancer Cancer, Case Western Reserve University, Biomedical Research Building#328, 2109 Adelbert Road, Cleveland, OH 44106, USA
| | - David Danielpour
- Case Comprehensive Cancer Cancer, Case Western Reserve University, Biomedical Research Building#328, 2109 Adelbert Road, Cleveland, OH 44106, USA
- Division of General Medical Sciences, Case Western Reserve University, Biomedical Research Building#328, 2109 Adelbert Road, Cleveland, OH 44106, USA
| | - Ricky Chan
- Institute for Computational Biology, Case Western Reserve University, Biomedical Research Building#328, 2109 Adelbert Road, Cleveland, OH 44106, USA
| | - Guang Zhou
- Department of Orthopaedics, Case Western Reserve University, Biomedical Research Building#328, 2109 Adelbert Road, Cleveland, OH 44106, USA
- Case Comprehensive Cancer Cancer, Case Western Reserve University, Biomedical Research Building#328, 2109 Adelbert Road, Cleveland, OH 44106, USA
- Department of Genetics and Genome Sciences, Case Western Reserve University, Biomedical Research Building#328, 2109 Adelbert Road, Cleveland, OH 44106, USA
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Shi D, Mu S, Hu B, Zhang S, Liu J, Zhang Z, Shao Z. Prognostic role of c-Jun activation domain-binding protein-1 in cancer: A systematic review and meta-analysis. J Cell Mol Med 2021; 25:2750-2763. [PMID: 33550701 PMCID: PMC7957274 DOI: 10.1111/jcmm.16334] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/08/2020] [Revised: 01/12/2021] [Accepted: 01/18/2021] [Indexed: 12/27/2022] Open
Abstract
c-Jun activation domain-binding protein-1 (Jab1) is aberrantly overexpressed in multiple cancers and plays an oncogenic role in cancer progression. We examined the association between Jab1 expression and prognosis in patients with cancer by conducting a meta-analysis. A comprehensive search strategy was performed using the PubMed, Web of Science, Ovid and EMBASE in July 2020. Eligible studies were enrolled according to definite criteria. Twenty-seven studies involving 2609 patients were enrolled in this meta-analysis. A significant association between high Jab1 expression and poor overall survival (pooled hazard ratio [HR] 2.344, 95% confidence interval [CI]: 2.037-2.696) was observed. Subgroup analyses of the type of cancer, sample size, follow-up period, Jab1 detection method and preoperative treatment did not alter the significance. On pooling data from Cox multivariate analyses, high Jab1 expression was found to be an independent prognostic indicator for overall survival. In addition, high Jab1 expression was found to be associated with advanced clinicopathological features such as clinical stage, lymphatic metastasis, histological grade and distant metastasis in cancers. Our meta-analysis is the first to demonstrate that high Jab1 expression may be a promising indicator of poor prognosis and has an independent prognostic value for overall survival in patients with cancer.
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Affiliation(s)
- Deyao Shi
- Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Shidai Mu
- Department of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Binwu Hu
- Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Shuo Zhang
- Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Jianxiang Liu
- Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Zhicai Zhang
- Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Zengwu Shao
- Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
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Wei J, Ma L, Lai YH, Zhang R, Li H, Li C, Lin J. Bazedoxifene as a novel GP130 inhibitor for Colon Cancer therapy. JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH : CR 2019; 38:63. [PMID: 30736824 PMCID: PMC6368818 DOI: 10.1186/s13046-019-1072-8] [Citation(s) in RCA: 45] [Impact Index Per Article: 7.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 02/26/2018] [Accepted: 01/30/2019] [Indexed: 12/22/2022]
Abstract
Background Interleukin-11 (IL-11), a dominant IL-6 family cytokine, is involved in tumorigenesis, tumor progression and differentiation in colon cancer cells. IL-11 signaling has been recently identified as a potential therapeutic target in colon cancer. Bazedoxifene, a third- generation selective estrogen modulator approved by the Food and Drug Administration (FDA), is a novel inhibitor of IL-11/GP130 signaling discovered by docking modeling. Methods In this study, the inhibition efficacy of bazedoxifene in colon cancer cells and its potential mechanism were investigated in vitro and in vivo by using MTT cell viability assay, BrdU cell proliferation assay, colony formation assay, wound-healing/cell migration assay, immunofluorescence, western blot assay and the mouse xenograft tumor model. Results Bazedoxifene inhibits phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) and its nuclear translocation induced by IL-11 in colon cancer cells. It also inhibits p-STAT3 induced by IL-6 and IL-11 but not by OSM or STAT1 phosphorylation induced by INF-γ in human colon cancer cells. In addition, bazedoxifene can significantly inhibit phosphorylation of AKT and STAT3 downstream targets. Furthermore, bazedoxifene alone or together with oxaliplatin can significantly induce apoptosis, inhibit cell viability, cell colony formation and cell migration in colon cancer cells. Knock-down of IL-11R can reduce the sensitivity of colon cancer cells to bazedoxifene. IL-11 can reduce the efficacy of oxaliplatin-mediated inhibition of cell viability. Consistent with in vitro findings, bazedoxifene alone also attenuated HCT-15 xenograft tumor burden and reduced p-STAT3, p-AKT and p-ERK in vivo. Its combination with oxaliplatin attenuated DLD-1 xenograft tumor burden and reduced p-STAT3 in vivo. Conclusions Taken together, these results support bazedoxifene as a novel and effective therapeutic agent targeting IL-11/GP130 signaling for human colorectal cancer therapy. Electronic supplementary material The online version of this article (10.1186/s13046-019-1072-8) contains supplementary material, which is available to authorized users.
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Affiliation(s)
- Jia Wei
- Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.,Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene Street, Baltimore, MD, 21201, USA
| | - Ling Ma
- Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene Street, Baltimore, MD, 21201, USA
| | - Yi-Hui Lai
- 33 Linsen Road, Chungshan District, Taipei, Taiwan
| | - Ruijie Zhang
- Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene Street, Baltimore, MD, 21201, USA
| | - Huameng Li
- Biophysics Graduate Program, The Ohio State University, Columbus, OH, 43210, USA
| | - Chenglong Li
- College of Pharmacy, University of Florida, Gainesville, FL, 32610, USA
| | - Jiayuh Lin
- Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene Street, Baltimore, MD, 21201, USA.
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Kang KA, Ryu YS, Piao MJ, Shilnikova K, Kang HK, Yi JM, Boulanger M, Paolillo R, Bossis G, Yoon SY, Kim SB, Hyun JW. DUOX2-mediated production of reactive oxygen species induces epithelial mesenchymal transition in 5-fluorouracil resistant human colon cancer cells. Redox Biol 2018; 17:224-235. [PMID: 29715584 PMCID: PMC6006906 DOI: 10.1016/j.redox.2018.04.020] [Citation(s) in RCA: 41] [Impact Index Per Article: 5.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/14/2018] [Revised: 04/16/2018] [Accepted: 04/18/2018] [Indexed: 02/07/2023] Open
Abstract
The therapeutic benefits offered by 5-fluorouracil (5-FU) are limited because of the acquisition of drug resistance, the main cause of treatment failure and metastasis. The ability of the cancer cells to undergo epithelial-mesenchymal transition (EMT) contributes significantly to cancer metastatic potential and chemo-resistance. However, the underlying molecular mechanisms of 5-FU-resistance have remained elusive. Here, we show that reactive oxygen species (ROS), produced by dual oxidase 2 (DUOX2), promote 5-FU-induced EMT. First, we showed that 5-FU–resistant SNUC5 colon cancer cells (SNUC5/FUR cells) undergo EMT by analyzing the expression of EMT markers such as N-cadherin, vimentin and E-cadherin. In addition, we found that the resistant cells expressed higher levels of Snail, Slug, Twist and Zeb1, which are all critical EMT regulators and had enhanced migratory and invasive capabilities. Furthermore, SNUC5/FUR cells had increased level of DUOX2, resulting in increased ROS level. This effect was due to the enhanced binding of the ten eleven translocation 1 (TET1) demethylase to the DUOX2 promoter in the SNUC5/FUR cells. Importantly, silencing of TET1 reversed the effects of 5-FU on the cells. Finally, the antioxidant N-acetylcysteine attenuated the effects of 5-FU on EMT and metastasis. Our study demonstrates the existence of a TET1/DUOX2/ROS/EMT axis that could play a role in colon cancer chemo-resistance and the aggressiveness of this cancer.
5-Fluorouracil (FU)-resistance is associated with epithelial-mesenchymal transition. ROS play a key role in EMT induction in 5-FU resistant colon cancer cells. 5-FU-resistant cells overexpress the DNA demethylase TET1, which binds to the promoter of the NADPH oxidase DUOX2 and induces its expression.
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Affiliation(s)
- Kyoung Ah Kang
- School of Medicine, Jeju National University, Jeju 63243, Republic of Korea
| | - Yea Seong Ryu
- School of Medicine, Jeju National University, Jeju 63243, Republic of Korea
| | - Mei Jing Piao
- School of Medicine, Jeju National University, Jeju 63243, Republic of Korea
| | | | - Hee Kyoung Kang
- School of Medicine, Jeju National University, Jeju 63243, Republic of Korea
| | - Joo Mi Yi
- Department of Microbiology and Immunology, Inje University College of Medicine, Busan 47392, Republic of Korea
| | - Mathias Boulanger
- Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, Montpellier, France
| | - Rosa Paolillo
- Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, Montpellier, France
| | - Guillaume Bossis
- Institut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, Montpellier, France
| | - Sung Young Yoon
- Plasma Technology Research Center of National Fusion Research Institute, 37, Dongjangsan-ro, Gunsan-si, Jeollabuk-do, Gunsan 54004, Republic of Korea
| | - Seong Bong Kim
- Plasma Technology Research Center of National Fusion Research Institute, 37, Dongjangsan-ro, Gunsan-si, Jeollabuk-do, Gunsan 54004, Republic of Korea
| | - Jin Won Hyun
- School of Medicine, Jeju National University, Jeju 63243, Republic of Korea.
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