Effect of METTL3 knockdown on MCF10 breast cancer progression model
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE237066 | GEO | 2023/11/20
REPOSITORIES: GEO
Similar Datasets
Project description:Effect of METTL3 knockdown on MCF10 breast cancer progression model
| PRJNA993659 | ENA
Project description:We assess the effect of METTL3 on gene expression and transcriptional splicing in three different human breast cancer cell lines
2022-07-01 | E-MTAB-11664 | biostudies-arrayexpress
Project description:Transcription and processing of histone mRNAs occurs at subnuclear domains known as Histone Locus Bodies (HLBs). Although it is known that higher-order chromatin organization is dysregulated in cancer, structural alterations within HLB across breast cancer progression are unclear. Differential expression across known as MCF10, a basal triple negative breast cancer progression model, followed by pathway analysis demonstrated many alterations in signaling cascades known to be related to proliferation. Positional gene enrichment identified the hist1 gene locus at chromosome 6p22 as the most significantly altered cluster of genes from the normal-like MCF10A to premalignant MCF10AT1. The malignant MCF10CA1a had a more varied expression pattern across the hist1 locus. Within this region there are three subclusters of hist1 genes which were generally upregulated while intervening genes were more frequently downregulated. Extending these findings to TCGA breast tumors revealed that normal adjacent tissue had lower expression within the subclusters than their matched tumor samples. Moreover, the expression pattern within the hist1 locus comparing normal versus tumors recapitulated a very similar pattern to that comparing 10A to AT1 or CA1a. Since the hist1 locus is transcribed and processed at a specific subnuclear microenvironment, the higher order chromatin organization of this locus may be a critical component of its regulation. We addressed whether CTCF, a key chromatin organizing protein, may play a role in organizing the hist1 HLB. Immunofluorescence for CTCF along with NPAT, a protein which decorates this locus, identified that CTCF may tether the hist1 HLB to the nuclear matrix. All three subclusters reside within a single topologically associating domain wherein interacting loops are bound by CTCF. Inter-subcluster interactions are lost in the premalignant AT1. Consistent with the varied expression across the hist1 HLB in CA1a, inter-subcluster interactions are regained in the malignant state. These data suggest a transient state in highly proliferative breast cancer cells in which the hist1 HLB is dynamically reorganized.
2017-05-23 | GSE98552 | GEO
Project description:Transcription and processing of histone mRNAs occurs at subnuclear domains known as Histone Locus Bodies (HLBs). Although it is known that higher-order chromatin organization is dysregulated in cancer, structural alterations within HLB across breast cancer progression are unclear. Differential expression across known as MCF10, a basal triple negative breast cancer progression model, followed by pathway analysis demonstrated many alterations in signaling cascades known to be related to proliferation. Positional gene enrichment identified the hist1 gene locus at chromosome 6p22 as the most significantly altered cluster of genes from the normal-like MCF10A to premalignant MCF10AT1. The malignant MCF10CA1a had a more varied expression pattern across the hist1 locus. Within this region there are three subclusters of hist1 genes which were generally upregulated while intervening genes were more frequently downregulated. Extending these findings to TCGA breast tumors revealed that normal adjacent tissue had lower expression within the subclusters than their matched tumor samples. Moreover, the expression pattern within the hist1 locus comparing normal versus tumors recapitulated a very similar pattern to that comparing 10A to AT1 or CA1a. Since the hist1 locus is transcribed and processed at a specific subnuclear microenvironment, the higher order chromatin organization of this locus may be a critical component of its regulation. We addressed whether CTCF, a key chromatin organizing protein, may play a role in organizing the hist1 HLB. Immunofluorescence for CTCF along with NPAT, a protein which decorates this locus, identified that CTCF may tether the hist1 HLB to the nuclear matrix. All three subclusters reside within a single topologically associating domain wherein interacting loops are bound by CTCF. Inter-subcluster interactions are lost in the premalignant AT1. Consistent with the varied expression across the hist1 HLB in CA1a, inter-subcluster interactions are regained in the malignant state. These data suggest a transient state in highly proliferative breast cancer cells in which the hist1 HLB is dynamically reorganized.
2017-05-23 | GSE98551 | GEO
Project description:label the cells overexpressed Myc tagged METTL3 and Flag tagged WTAP with 4-SU, the RNA bound by METT3,WTAP can be got by Myc or Flag IP followed by RNA isolation by using the TRIzol (Invitrogen) reagent by following the company manual.the RNA was then used for library preparation using a TruSeq™ RNA Sample Prep Kit v2 (Illumina, San Diego, CA, USA) according to the manufacturer’s protocol.The libraries were sequenced using HiSeq2000 (Illumina) in single-read mode, creating reads with a length of 50 bp. Sequencing chemistry v2 (Illumina) was used and samples were multiplexed in two samples per lane. discovery of the binding motif of METTL3，WTAP in METTL3，WTAP overexpressed Human 293T cells
2014-01-16 | E-GEOD-50580 | biostudies-arrayexpress
Project description:MCF10AT1 (M-II), MCF10CA1h (M-III) and MCF10CA1a.cl1 (M-IV) are a set of human breast cancer cell lines that derived from the same parent cell line MCF10 but display distinct phenotypes in metastatic potential in the form of xenografts in immune-compromised mice. From M-II to M-IV, the metastatic potential is gradually increased. Using a self-designed real-time PCR based miRNA array containing 242 genes, we tested the miRNA expression levels in these cell lines in order to identify metastasis-related miRNAs.
2012-12-13 | GSE42884 | GEO
Project description:we find METTL3 associates with polyribosomes and promotes translation. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to the 3' untranslated region (UTR) of a reporter mRNA. Mechanistically, METTL3 enhances mRNA translation through an interaction with the translation initiation machinery. m6A seq in A549 and H1299 cells, RNA seq in METTL3 knockdown cells
2016-07-03 | E-GEOD-76367 | biostudies-arrayexpress
Project description:METTL3 and METTL14 are considered to faithfully form the m6A writing complex in a 1:1 ratio, regulating the fate of mRNA by adding m6A modifications. However, recent studies have shown inconsistent expression and prognostic value of METTL3 and METTL14 in some tumors, suggesting that they may not be faithful in tumors. Pan-cancer analysis based on TCGA data reveals significant differences in expression, function, tumor burden correlation, and immune correlation between METTL3 and METTL14, especially in esophageal squamous cell carcinoma (ESCC). Knockdown of METTL3 significantly inhibits the cell proliferation in vitro and in vivo in ESCC EC109 cells, while the impact of METTL14 knockdown on proliferation is limited, and it cannot abolish the expression of METTL3 protein. mRNA-seq results indicate that METTL3 independently regulates the expression of 1615 genes, while only 776 genes are co-regulated by METTL3 and METTL14. Furthermore, through immunofluorescence co-localization, it is observed that METTL3 and METTL14 have certain inconsistencies in cellular localization. HPLC-MS results show that METTL3 independently binds to the Nop56p-associated pre-rRNA complex and mRNA splicing complex, separate from METTL14. Through bioinformatics and various omics studies, we have preliminarily discovered that METTL3 independently regulating tumor cell proliferation, and the participation in mRNA splicing may be a critical molecular mechanism. Our study provides an experimental basis and theoretical foundation for further understanding of the m6A writing complex and tumor therapy targeting METTL3.
2024-02-01 | PXD048886 | Pride
Project description:To gain insight into possible processes that require m6A for their function, METTL3 was knocked down (KD) in HepG2 cells by siRNA transfections Differential expression analysis of METTL3 KD versus mock-transfected HepG2 cells, in 2 biological replicates
2012-04-25 | E-GEOD-37001 | biostudies-arrayexpress
Project description:We have used RNA-seq to explore gene expression profiles in scramble and METTL3 Knockdown HUVEC cell lines.
2021-12-01 | GSE157544 | GEO