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000303472 1001_ $$aPhoyen, Suchittra$$b0
000303472 245__ $$aMACC1 Expression in Colorectal Cancer Is Upregulated by Loss of Epigenetic Repression Under Oxidative Stress Condition.
000303472 260__ $$aNew York, NY [u.a.]$$bWiley$$c2025
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000303472 520__ $$aReactive oxygen species (ROS) cause oxidative stress and contribute to cancer genesis and progression. Metastasis-associated in colon cancer 1 (MACC1) is a key metastasis-mediating transcription factor in colorectal cancer (CRC). Whether ROS epigenetically regulated MACC1 expression and increased tumor progression in CRC have not been elucidated so far. We applied oxidative stress in two CRC cell lines with differential MACC1 expression (HCT116 and SW480) and analyzed the distribution of the histone marks H3K4me3 (active) and H4K20me3 (repressive), as well as the expression of MACC1. Alteration in cell motility by ROS was assayed with Boyden chambers. Abundance of H4K20me3 on the MACC1 promoter was determined by ChIP-seq. Induced oxidative stress in SW480 and HCT116 cells increased MACC1 mRNA and protein expression and enhanced cell migration. In the low MACC1 expression SW480 cells, oxidative stress resulted in a higher abundance of the active histone mark H3K4me3, and a lower abundance of repressive mark H4K20me3, both overall and specifically on the MACC1 promoter, compared with the medium MACC1 expression HCT116 cells. Analysis of histological abundances of H3K4me3 and H4K20me3 marks in a small panel of human CRC tumors showed an inverse correlation of H4K20me3 with MACC1. Experimentally, inhibition of H4K20me3 formation caused increased MACC1 mRNA expression in HCT116 cells. Conclusions, we reported a potential ROS-mediated epigenetic regulation of MACC1 expression in CRC through altered histone methylation, as our data suggested an initial epigenetic silencing of MACC1, which was later partially reactivated under oxidative stress.
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000303472 650_7 $$2Other$$aH4K20me3
000303472 650_7 $$2Other$$aMACC1
000303472 650_7 $$2Other$$aROS
000303472 650_7 $$2Other$$acolorectal cancer
000303472 650_7 $$2Other$$atumor progression
000303472 650_7 $$2NLM Chemicals$$aMACC1 protein, human
000303472 650_7 $$2NLM Chemicals$$aTranscription Factors
000303472 650_7 $$2NLM Chemicals$$aTrans-Activators
000303472 650_7 $$2NLM Chemicals$$aHistones
000303472 650_7 $$2NLM Chemicals$$aReactive Oxygen Species
000303472 650_2 $$2MeSH$$aHumans
000303472 650_2 $$2MeSH$$aOxidative Stress: drug effects
000303472 650_2 $$2MeSH$$aColorectal Neoplasms: pathology
000303472 650_2 $$2MeSH$$aColorectal Neoplasms: metabolism
000303472 650_2 $$2MeSH$$aColorectal Neoplasms: genetics
000303472 650_2 $$2MeSH$$aTranscription Factors: genetics
000303472 650_2 $$2MeSH$$aTranscription Factors: metabolism
000303472 650_2 $$2MeSH$$aTrans-Activators
000303472 650_2 $$2MeSH$$aEpigenesis, Genetic
000303472 650_2 $$2MeSH$$aUp-Regulation: drug effects
000303472 650_2 $$2MeSH$$aHistones: metabolism
000303472 650_2 $$2MeSH$$aCell Movement: drug effects
000303472 650_2 $$2MeSH$$aReactive Oxygen Species: metabolism
000303472 650_2 $$2MeSH$$aCell Line, Tumor
000303472 650_2 $$2MeSH$$aGene Expression Regulation, Neoplastic
000303472 650_2 $$2MeSH$$aHCT116 Cells
000303472 650_2 $$2MeSH$$aPromoter Regions, Genetic
000303472 7001_ $$0P:(DE-He78)d7c5b56f8fe865129d5c6161348ccf0b$$aDahlmann, Mathias$$b1
000303472 7001_ $$aHerrmann, Pia$$b2
000303472 7001_ $$00000-0002-6515-4321$$aBoonla, Chanchai$$b3
000303472 7001_ $$0P:(DE-HGF)0$$aStein, Ulrike$$b4
000303472 773__ $$0PERI:(DE-600)1496553-7$$a10.1002/cbf.70107$$gVol. 43, no. 8, p. e70107$$n8$$pe70107$$tCell biochemistry and function$$v43$$x0263-6484$$y2025
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