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The m6A reader HNRNPC promotes non-small cell lung cancer progression by enhancing E2F2 mRNA stability

ABSTRACT: The m6A reader HNRNPC promotes non-small cell lung cancer progression by enhancing E2F2 mRNA stability

PROVIDER: PRJNA1047148 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27006184_1.fastq.gz	Fastqsanger.gz
	SRR27006184_2.fastq.gz	Fastqsanger.gz
	SRR27006185_1.fastq.gz	Fastqsanger.gz
	SRR27006185_2.fastq.gz	Fastqsanger.gz

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The m6A reader HNRNPC promotes glioma progression by enhancing the stability of IRAK1 mRNA through the MAPK pathway

Project description:Glioma is the most common and aggressive primary malignant brain tumor. N6-methyladenosine (m6A) modification widely exists in eukaryotic cells and plays an important role in the occurrence and development of human tumors. Here, we show that the m6A reader HNRNPC was overexpression and related to poor prognosis in glioma patients. HNRNPC plays crucial role in glioma cell proliferation, invasion and tumorigenesis. HNRNPC augments m6A-dependent mRNA stability of IRAK1, which impacted poor survival for glioma patients, further activated the downstream MAPK pathway. HNRNPC promotes glioma cells progression largely through the upregulation of IRAK1. Together, our findings demonstrate the novel HNRNPC-IRAK1-MAPK axis critical for glioma tumorigenesis and extend the reason for the upregulation of IRAK1.

2024-06-12 | GSE245688 | GEO

The m6A reader HNRNPC promotes non-small cell lung cancer progression by enhancing E2F2 mRNA stability

Project description:HNRNPC, as one of the m6A reading proteins, has been confirmed to be highly expressed in a variety of tumors and promote the occurrence and progression of tumors. Previous studies have confirmed that HNRNPC significantly promoted the proliferation, migration and invasion of NSCLC cells, and its high expression was related to the clinical stage, lymph node and distant metastasis of patients, and could be used as an indicator of poor prognosis of NSCLC. However, the role of HNRNPC in regulating gene expression through m6A methylation modification in the occurance and progression of NSCLC remains largely unexplored. To investigate the target genes bound by HNRNPC, samples from A549 cells were harvested by RIP lysis buffer, and then the lysates were immunoprecipitated by 5μg anti-HNRNPC antibody. finally, the potential target genes were identified by RIP-seq.

2023-12-05 | GSE249094 | GEO

The m6A reader HNRNPC promotes glioma progression by enhancing the stability of IRAK1 mRNA through the MAPK pathway

Project description:The m6A reader HNRNPC promotes glioma progression by enhancing the stability of IRAK1 mRNA through the MAPK pathway

| PRJNA1029580 | ENA

Structural basis of YTH domain as m6A reader

Project description:The N6-methyladenosine (m6A) is the most abundant internal modification in almost all eukaryotic messenger RNAs, and is dynamically regulated. Therefore, identification of m6A readers is especially important in determining the cellular function of m6A. YTHDF2 has recently been characterized as the first m6A reader that regulates the cytoplasmic stability of methylated RNA. Here we show that YTHDC1 is a nuclear m6A reader and report the crystal structure of the YTH domain of YTHDC1 bound to m6A-containing RNA. We further determined the structure of another YTH domain, YTHDF1, and found that the YTH domain utilizes a conserved aromatic cage to specifically recognize the methyl group of m6A. Our structural characterizations of the YTHDC1-m6A RNA complex also shed light on the molecular basis for the preferential binding of the GG(m6A)C sequence by YTHDC1 and confirm the YTH domain as a specific m6A RNA reader. PAR-CLIP (Photoactivatable-Ribonucleoside-Enhanced Crosslinking and Immunoprecipitation) was applied to human YTHDC1 protein to identify its binding sites.

2014-09-18 | E-GEOD-58352 | biostudies-arrayexpress

The m6A reader IGF2BP3 promotes acute myeloid leukemia progression by enhancing RCC2 stability.

Project description:N6-methyladenosine (m6A) is the most abundant posttranscriptional modification of mRNA in eukaryotes. Recent evidence suggests that dysregulated m6A-associated proteins and m6A modifications play a pivotal role in the initiation and progression of diseases such as cancer. Here, we identified that IGF2BP3 is specifically overexpressed in acute myeloid leukemia (AML), a subtype of leukemia associated with poor prognosis and high genetic risk. IGF2BP3 is required for maintaining AML cell survival in an m6A-dependent manner, and knockdown of IGF2BP3 dramatically suppresses the apoptosis, reduces the proliferation, and impairs the leukemic capacity of AML cells in vitro and in vivo. Mechanistically, IGF2BP3 interacts with RCC2 mRNA and stabilizes the expression of m6A-modified RNA. Thus, we provided compelling evidence demonstrating that the m6A reader IGF2BP3 contributes to tumorigenesis and poor prognosis in AML and can serve as a target for the development of cancer therapeutics.

| S-EPMC8894383 | biostudies-literature

hNRNPC iCLIP

Project description:hNRNPC iCLIP

| PRJEB2253 | ENA

Structural basis of YTH domain as m6A reader

2014-09-18 | GSE58352 | GEO

Transcriptome profiling of cells depleted of hnRNPC, Upf1, or co-depleted of hnRNPC and Upf1.

Project description:The purpose of this experiment was to compare differences in Alu-exon inclusion in cells depleted of hnRNPC, Upf1, or both.

2016-04-01 | E-MTAB-4008 | biostudies-arrayexpress

Differentially expressed genes in HNRNPC knockdown MHCC97H cells

Project description:HNRNPC plays an important role in HCC metastasis, HNRNPC knockdown by specific shRNA (HNRNPC-shRNA) significantly inhibited the migration and invasion of MHCC97H cells, while HNRNPC overexpression exerted the opposite effect. To elucidate the mechanisms by which HNRNPC facilitated HCC metastasis, we performed microarray analysis to compare the transcription profiling between the MHCC97H-shcontrol and MHCC97H-shHNRNPC cells.

2022-07-27 | GSE180789 | GEO

hnRNPC regulates cancer-specific alternative cleavage and polyadenylation profiles

Project description:Alternative cleavage and polyadenylation (APA) can occur at more than half of all human genes, greatly enhancing the cellular repertoire of mRNA isoforms. As these isoforms can have altered stability, localisation and coding potential, deregulation of APA can disrupt gene expression and this has been linked to many diseases including cancer progression. How APA generates cancer-specific isoform profiles and what their physiological consequences are, however, is largely unclear. Here we use a subcellular fractionation approach to determine the nuclear and cytoplasmic APA profiles of successive stages of colon cancer using a cell line-based model. Using this approach, we show that during cancer progression specific APA profiles are established. We identify that overexpression of hnRNPC has a critical role in the establishment of APA profiles characteristic for metastatic colon cancer cells, by regulating poly(A) site selection in a subset of genes that have been implicated in cancer progression including MTHFD1L.

2019-06-01 | GSE102357 | GEO

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