CCDC12 regulates selective shear of RBM47 to promote breast cancer progression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1111071 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29009324_1.fastq.gz | Fastqsanger.gz | |||
| SRR29009324_2.fastq.gz | Fastqsanger.gz | |||
| SRR29009325_1.fastq.gz | Fastqsanger.gz | |||
| SRR29009325_2.fastq.gz | Fastqsanger.gz | |||
| SRR29009326_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: TThe Coiled coil domain containing (CCDC) protein is an egg that is closely related to malignant tumors. Methods:Breast cancer cells MDA-MB-231(NC), MDA-MB-231(shCCDC12)were deeply sequenced by Illumina sequencing platform (HISEQ2500) in triplices. Genes with adjusted p values < 0.05 and |foldChange| > 2 were defined as differential expression Genes (DEGs) and enriched with GO and KEGG. Several essential genes were validated by qRT-PCR using QuantStudio 5 (Thermo Fisher) and SYBR Green assays. The White Family. Studies have shown that CCDC protein is abnormally expressed in malignant tumors and changes cell proliferation cycle by regulating cell transcription factors Stage, promote the invasion and metastasis of malignant tumor cells. How does CCDC12 as a shear gene affect the biology of breast cancer Scientific activity remains to be further studied. Results: To verify the biological properties of CCDC12 in breast cancer, we studied breast cancer MDA-MB-231 knocked down the expression of CCDC12 in the cell line, and previous studies showed that TCGA and CPTAC database scores The mRNA and protein expression levels of CCDC12 gene were significantly up-regulated in normal breast cancer tissues compared with tumor tissues. Knocking down the expression level of CCDC12 in MDA-MB-231 cells can significantly inhibit cell growth, proliferation and migration. In tumor formation experiments in nude mice, low expression of CCDC12 can inhibit tumor growth. Knock down CCDC12 on MDA-MB-231 Splicing event analysis was performed by cell transcriptome sequencing, and differential analysis found that CCDC12 expression was differentially induced in breast cancer cells The RNA binding motif protein 47 (RBM47) Skipped exon, causing RMB47 to open The structure of the reading frame changes, altering gene function. Conclusions:This study confirmed that CCDC12 regulates the invasion and metastasis of breast cancer cells by regulating the variable shear of RBM47, inducing cell cycle arrest and promoting cell apoptosis. The results of RNA-Seq were consistent with our in vitro and in vivo experiments.
2024-12-31 | GSE267326 | GEO
Project description:Through integrative analysis of clinical breast cancer gene expression datasets, cell line models of breast cancer progression, and mutation data from cancer genome resequencing studies, we have identified RNA binding motif protein 47 (RBM47) as a candidate suppressor of breast cancer metastasis. RBM47 inhibited breast cancer progression in experimental models. Transcriptome-wide analysis of RBM47 localization by HITS-CLIP revealed widespread binding to mRNAs, preferentially at the 3' UTRs. RBM47 altered the abundance of a subset of its target mRNAs. Some of the mRNAs stabilized by RBM47, as exemplified by dickkopf WNT signaling pathway inhibitor 1 (DKK1), mediate tumor suppressive effects downstream of RBM47. This work identifies RBM47 as a suppressor of breast cancer progression and highlights the potential of global RNA modulatory events as a source of metastasis-promoting phenotypic traits. Cancer cells transduced with doxycycline-inducible wildtype RBM47 or the RBM47-I281fs mutant, treated with increasing concentrations of doxycycline.
2014-06-11 | E-GEOD-53779 | biostudies-arrayexpress
Project description:Through integrative analysis of clinical breast cancer gene expression datasets, cell line models of breast cancer progression, and mutation data from cancer genome resequencing studies, we have identified RNA binding motif protein 47 (RBM47) as a candidate suppressor of breast cancer metastasis. RBM47 inhibited breast cancer progression in experimental models. Transcriptome-wide analysis of RBM47 localization by HITS-CLIP revealed widespread binding to mRNAs, preferentially at the 3' UTRs. RBM47 altered the abundance of a subset of its target mRNAs. Some of the mRNAs stabilized by RBM47, as exemplified by dickkopf WNT signaling pathway inhibitor 1 (DKK1), mediate tumor suppressive effects downstream of RBM47. This work identifies RBM47 as a suppressor of breast cancer progression and highlights the potential of global RNA modulatory events as a source of metastasis-promoting phenotypic traits.
2014-06-11 | GSE53779 | GEO
Project description:We identified RNA binding motif protein 47 (RBM47) as a target gene of transforming growth factor (TGF)-beta in mammary gland epithelial cells (NMuMG cells) that have undergone the epithelial-to-mesenchymal transition (EMT). TGF-beta repressed RBM47 expression in NMuMG cells and lung cancer cell lines. Expression of RBM47 correlated with good prognosis in patients with lung, breast, and gastric cancer. RBM47 suppressed the expression of cell metabolism-related genes, which were the direct targets of nuclear factor erythroid 2-related factor 2 (Nrf2; also known as NFE2L2). RBM47 bound to KEAP1 and Cullin3 mRNAs, and knockdown of RBM47 inhibited their protein expression, which led to enhanced binding of Nrf2 to target genomic regions. Knockdown of RBM47 also enhanced the expression of some Nrf2 activators, p21/CDKN1A and MafK induced by TGF-beta. Both mitochondrial respiration rates and the side population cells in lung cancer cells increased in the absence of RBM47. Our findings, together with the enhanced tumor formation and metastasis of xenografted mice by knockdown of the RBM47 expression, suggested tumor suppressive roles for RBM47 through the inhibition of Nrf2 activity. Effect of shRNA for RBM47 and TGF-beta on gene expression was evaluated by RNA-seq and RBM47-bound RNAs were identified by RIP-seq in A549 cells.
2016-03-01 | E-GEOD-61910 | biostudies-arrayexpress
Project description:We identified RNA binding motif protein 47 (RBM47) as a target gene of transforming growth factor (TGF)-beta in mammary gland epithelial cells (NMuMG cells) that have undergone the epithelial-to-mesenchymal transition (EMT). TGF-beta repressed RBM47 expression in NMuMG cells and lung cancer cell lines. Expression of RBM47 correlated with good prognosis in patients with lung, breast, and gastric cancer. RBM47 suppressed the expression of cell metabolism-related genes, which were the direct targets of nuclear factor erythroid 2-related factor 2 (Nrf2; also known as NFE2L2). RBM47 bound to KEAP1 and Cullin3 mRNAs, and knockdown of RBM47 inhibited their protein expression, which led to enhanced binding of Nrf2 to target genomic regions. Knockdown of RBM47 also enhanced the expression of some Nrf2 activators, p21/CDKN1A and MafK induced by TGF-beta. Both mitochondrial respiration rates and the side population cells in lung cancer cells increased in the absence of RBM47. Our findings, together with the enhanced tumor formation and metastasis of xenografted mice by knockdown of the RBM47 expression, suggested tumor suppressive roles for RBM47 through the inhibition of Nrf2 activity.
2016-03-01 | GSE61910 | GEO
Project description:RBM47 Inhibits Hepatocellular Carcinoma Progression as a DNA/RNA Regulator
| PRJNA833425 | ENA
Project description:After ChIP assay, DNA sequencing was conducted to analyze the specific loci binding by RBM47 in HCCLM3 cells.
2025-04-28 | GSE201818 | GEO
Project description:ABSTRACT RNA binding motif proteins (RBMs) have been widely implicated in the tumorigenesis of multiple human cancers, but scarcely studied in nasopharyngeal carcinoma (NPC). Here, we compare the mRNA levels of 29 RBMs between 87 NPC and 10 control samples. We find that RBM47 is frequently upregulated in NPC specimens and its high expression is associated with poor prognosis of patients with NPC. Biological experiments show that RBM47 plays an oncogenic role in NPC cells. Mechanically, RBM47 binds to the promoter and regulates the transcription of BCAT1 and its overexpression partially rescues the inhibitory effects of RBM47-knockdown on NPC cells. Moreover, transcriptome analysis reveals that RBM47 regulates alternative splicing of pre-mRNA, including those cancer-related, to a large extent in NPC cells. Furthermore, RBM47 binds to hnRNPM and cooperativelyjointly regulates multiple splicing events in NPC cells. In addition, we find that knockdown of hnRNPM inhibits proliferation and migration of NPC cells. Taken together, our study shows that RBM47 promotes the progression of NPC through multiple pathways, acting as a transcriptional factor and a modulator of alternative splicing in cooperation with hnRNPM. Our study also highlights that RBM47 and hnRNPM could be prognostic factors and potential therapeutic targets for NPC. Keywords RBM47, BCAT1, Alternative splicing, hnRNPM, Nasopharyngeal Carcinoma (NPC)
2022-06-01 | GSE176549 | GEO
Project description:By RIP sequencing, we determined that RBM47 modulated UPF1 by stabilizing its mRNA and addressed the novel motif in the UPF1 3’UTR with direct binding.
2025-04-28 | GSE201892 | GEO
Project description:The experimental purpose is to investigate the protein interactions involving RBM47 through mass spectrometry experiments.
2023-12-01 | PXD045984 | Pride