KDM5B histone demethylase controls epithelial-mesenchymal transition of cancer cells by regulating the expression of the microRNA-200 family

Enkhbaatar, Zanabazar; Terashima, Minoru; Oktyabri, Dulamsuren; Tange, Shoichiro; Ishimura, Akihiko; Yano, Seiji; Suzuki, Takeshi

doi:10.4161/cc.25142

Cited by 66 publications

(98 citation statements)

References 40 publications

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“…Previously, we reported that KDM5B, an H3K4 demethylase, down-regulated the expression of KAT5 and CD82 genes to increase cell invasion [6] and repressed the expression of microRNA-200 (miR-200) family, thereby promoting epithelial-mesenchymal transition (EMT) of cancer cells [7]. Thus our studies indicated that histone methyl-modifying enzymes were involved not only in tumor initiation but also in tumor progression.…”

Section: Introductionmentioning

confidence: 87%

“…The plasticity of EMT suggests that epigenetic regulation such as DNA methylation, histone modification and microRNA may be involved in EMT program [11]. There are several papers including our study demonstrating the connection between E-cadherin repression and the function of histone methyl-modifying enzymes [7,12,13]. However, the role of histone methylation in EMT is just beginning to be disclosed.…”

Section: Introductionmentioning

confidence: 98%

“…The enrichment of the specific amplified region was analyzed by QPCR and percentage enrichment of each histone modification over input chromatin DNA was shown. previously [7].…”

Section: Chromatin Immunoprecipitation (Chip) Assaysmentioning

confidence: 99%

“…A549 human lung cancer cell line and HT29 colon cancer cell line were maintained as described previously [7]. For EMT induction, the cells were treated with 1 to 5 ng/ml of TGF-β (R&D Systems) for 24 to 72 hours.…”

Section: Rt-pcr (Qrt-pcr) (Supplementarymentioning

confidence: 99%

“…P-values were calculated between control and the samples using Student's t-test. Primers used for the QPCR were described previously [6,7] and listed in Supplementary Table S1. The primers for human EED could also detect mouse EED transcripts.…”

Section: Quantitative Pcrmentioning

confidence: 99%

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EED regulates epithelial–mesenchymal transition of cancer cells induced by TGF-β

Oktyabri

Tange

Terashima

et al. 2014

Biochemical and Biophysical Research Communications

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Histone methylation is involved in various biological and pathological processes including cancer development. In this study, we found that EED, a component of Polycomb family genes through the regulation of histone H3 methylation and EZH2 occupancies on their regulatory regions. Our study demonstrated a novel role of EED, which regulates PRC2 activity and histone methylation during TGF-β-induced EMT of cancer cells.

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Section: Introductionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 98%

“…The enrichment of the specific amplified region was analyzed by QPCR and percentage enrichment of each histone modification over input chromatin DNA was shown. previously [7].…”

Section: Chromatin Immunoprecipitation (Chip) Assaysmentioning

confidence: 99%

Section: Rt-pcr (Qrt-pcr) (Supplementarymentioning

confidence: 99%

Section: Quantitative Pcrmentioning

confidence: 99%

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EED regulates epithelial–mesenchymal transition of cancer cells induced by TGF-β

Oktyabri

Tange

Terashima

et al. 2014

Biochemical and Biophysical Research Communications

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Dynamic regulation of tumour progression by phenotype‐switching drivers

Vock

Gschwendtner

Eckel

et al. 2022

Clinical & Translational Med

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BACKGROUNDFor decades, researchers have strived to analyze the process of tumour formation and progression. Despite the immense accumulation of knowledge, cancer still remains one of the biggest burdens of our society today. According to the WHO, nearly one in six deaths worldwide was attributed to cancer in 2020. Hence, it is crucial to revisit and build upon recent achievements to improve our understanding of this disease.One of the most important concepts to describe the growth and spreading of tumour cells in patients over time is the phenotype-switching model. 1 This model was first discovered in melanoma and is also applicable to other tumours. It is based on the idea that tumour cells can exist in two different cellular states. On the one hand, they exhibit a high proliferative activity with a high rate of glycolysis, but low migrative and invasive capacity. On the other hand, cells can exist in a state hallmarked by up-regulation of migrative and invasive behaviour with inflammation-related pathways being increased. Therefore, increasing evidence supports the idea that tumours progress to metastasis by dynamically switching from a local, proliferative state to a highly migrative state, whichThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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HPV16 E7‐induced upregulation of KDM2A promotes cervical cancer progression by regulating miR‐132–radixin pathway

Zhu

Zhao

et al. 2018

Journal Cellular Physiology

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KDM5B histone demethylase controls epithelial-mesenchymal transition of cancer cells by regulating the expression of the microRNA-200 family

Cited by 66 publications

References 40 publications

EED regulates epithelial–mesenchymal transition of cancer cells induced by TGF-β

EED regulates epithelial–mesenchymal transition of cancer cells induced by TGF-β

Dynamic regulation of tumour progression by phenotype‐switching drivers

HPV16 E7‐induced upregulation of KDM2A promotes cervical cancer progression by regulating miR‐132–radixin pathway

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