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Keratin 19 binds and regulates cytoplasmic HNRNPK mRNA targets in triple-negative breast cancer

ABSTRACT: Keratin 19 binds and regulates cytoplasmic HNRNPK mRNA targets in triple-negative breast cancer

PROVIDER: PRJNA926958 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23199821.fastq.gz	Fastqsanger.gz
	SRR23199822.fastq.gz	Fastqsanger.gz
	SRR23199823.fastq.gz	Fastqsanger.gz
	SRR23199824.fastq.gz	Fastqsanger.gz
	SRR23199825.fastq.gz	Fastqsanger.gz

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Keratin 19 binds and regulates cytoplasmic HNRNPK mRNA targets in triple-negative breast cancer.

Project description:BackgroundHeterogeneous nuclear ribonucleoprotein K (HNRNPK) regulates pre-mRNA processing and long non-coding RNA localization in the nucleus. It was previously shown that shuttling of HNRNPK to the cytoplasm promotes cell proliferation and cancer metastasis. However, the mechanism of HNRNPK cytoplasmic localization, its cytoplasmic RNA ligands, and impact on post-transcriptional gene regulation remain uncharacterized.ResultsHere we show that the intermediate filament protein Keratin 19 (K19) directly interacts with HNRNPK and sequesters it in the cytoplasm. Correspondingly, in K19 knockout breast cancer cells, HNRNPK does not localize in the cytoplasm, resulting in reduced cell proliferation. We comprehensively mapped HNRNPK binding sites on mRNAs and showed that, in the cytoplasm, K19-mediated HNRNPK-retention increases the abundance of target mRNAs bound to the 3' untranslated region (3'UTR) at the expected cytidine-rich (C-rich) sequence elements. Furthermore, these mRNAs protected by HNRNPK in the cytoplasm are typically involved in cancer progression and include the p53 signaling pathway that is dysregulated upon HNRNPK knockdown (HNRNPK KD) or K19 knockout (KRT19 KO).ConclusionsThis study identifies how a cytoskeletal protein can directly regulate gene expression by controlling the subcellular localization of RNA-binding proteins to support pathways involved in cancer progression.

| S-EPMC10433649 | biostudies-literature

Keratin 19 binds and regulates cytoplasmic HNRNPK mRNA targets in triple-negative breast cancer

Project description:This study identifies how a cytoskeletal protein can directly regulate gene expression by controlling the subcellular localization of RNA-binding proteins to support pathways involved in cancer progression.

2023-07-06 | GSE223603 | GEO

hnRNPK knock down in Ewing cell line

Project description:Ewing sarcoma is a highly aggressive tumor characterized by a translocation between members of the FET family of RNA binding proteins and one of several ETS transcription factors, with the most common translocation being EWS-FLI1. EWS-FLI1 leads to changes in gene expression through mechanisms that are not completely understood. We performed RNA sequencing analysis on primary pediatric human mesenchymal progenitor cells (pMPCs) expressing EWS-FLI1 in order to identify novel target genes. This analysis identified lnc277 as a previously uncharacterized long non-coding RNA upregulated by EWS-FLI1 in pMPCs. Inhibiting the expression of lnc277 diminished the ability of Ewing sarcoma cell lines to proliferate and form colonies in soft agar whereas inhibiting lnc277 had no effect on other cell types tested. By analyzing gene expression after shRNA knockdown, we found that both EWS-FLI1 and lnc277 repressed many more genes that they induced and that a significant fraction of EWS-FLI1 repressed targets were also repressed by lnc277. Analysis of primary human Ewing sarcoma RNA sequencing data further supports a role for lnc277 in mediating gene repression. We identified hnRNPK as an RNA binding protein that interacts directly with lnc277. We found a significant overlap in the genes repressed by hnRNPK and those repressed by both EWS-FLI1 and lnc277, suggesting that hnRNPK participates in lnc277 mediated gene repression. Thus, lnc277 is a previously uncharacterized long non-coding RNA downstream of EWS-FLI1 that facilitates the development of Ewing sarcoma via the repression of target genes. Our studies identify a novel mechanism of oncogenesis downstream of a chromosomal translocation and underscore the importance of lncRNA-mediated gene repression as a mechanism of EWS-FLI1 transcriptional regulation. A673 Ewing cells expressing an shRNA targeting hnRNPK or control were subjected to paired end RNA sequencing and compared to shGFP control.

2014-11-01 | E-GEOD-60890 | biostudies-arrayexpress

Analysis of nucleus and cytoplasm-specific HNRNPK binding on SINEUP RNA by seCLIP

Project description:To check the subcellular location-specific HNRNPK binding sites on mouse SINEB2 repeat element, we prepared seCLIP (single-end enhanced crosslinking and immunoprecipitation assay) libraries from SINEUP-GFP transfected nuclear and cytoplasmic fractions from HEK293T/17 cells.

2023-03-16 | GSE227250 | GEO

Expression data from Minoxdil, Keratin and microsphere keratin in vivo

Project description:Gene expression profiling reveals a potential effect of microsphere keratin in stimulating hair growth in vivo Mice back was depilated and then treated with 1% milliQ, 1% minoxidil, 1% keratin, 1% microsphere keratin for 20 days. Then the skin was collected and RNA was extracted from thetreatd skin as explained in the following section. The microarray was conducted for two biological replicates

2022-11-15 | GSE217935 | GEO

Effect of overexpressing HNRNPK in glioblastoma stem cell

Project description:The mechanisms underlys GBM cellular transitions remain unclear.In our study, we overexpressed HNRNPK in three different types of GSCs. HNRNPK (WT) leads to high expression of core markers in GSCs, and its characteristics are similar to those of the MES subtype, exhibiting stronger invasive abilities and tumorigenic potential. We mutated 422 site from lysine(K) to argnine(R) to study the function of SUMOylation in HNRNPK. Sequencing of GSCs with overexpression of HNRNPK (K422R) mutation confirmed the upregulation of infiltrating markers within the GSCs. The changes in GSC subtypes driven by overexpression of HNRNPK (WT or K422R) were not restricted by GSC mutation features.

2024-12-13 | GSE262681 | GEO

Expression data from Minoxdil, Keratin and microsphere keratin in vivo

Project description:Expression data from Minoxdil, Keratin and microsphere keratin in vivo

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Next Generation Sequencing Analysis of control and hnRNPK-/- RKO cells Transcriptomes

Project description:We generated the hnRNPK-/- RKO cells,and collected the cells at 2 days after transfectd with siRNA. Then,we extracted RNAs and performed next generation sequencing. By comparing sequcing data from control and hnRNPK -/- samples, we profiled the alternative splicing events and gene expression regulated by hnRNPK in CRC.

2018-10-26 | GSE85522 | GEO

Hnrnpk orchestrates embryonic growth plate development via regulating glycolysis

Project description:Here we show a multifunctional protein, Hnrnpk, is essential for preventing excessive apoptosis and premature differentiation of growth plate chondrocytes. These datas were the RNA-seq of E18.5 growth plate chondrocytes with or without Hnrnpk.

2022-09-28 | GSE197283 | GEO

Next Generation Sequencing Analysis of Wild Type and hnRNPK-MKO liver transcription

Project description:we report liver fibrosis defects in hnRNPK Alb-Cre mice, in which hnRNPK is ablated in hepatocyte cells.

2024-06-10 | GSE176594 | GEO