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KSHV Reprograms Host RNA Splicing via FAM50A to Activate STAT3 and Drive Oncogenic Cellular Transformation

ABSTRACT: KSHV Reprograms Host RNA Splicing via FAM50A to Activate STAT3 and Drive Oncogenic Cellular Transformation

PROVIDER: PRJNA1254174 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33252931_1.fastq.gz	Fastqsanger.gz
	SRR33252931_2.fastq.gz	Fastqsanger.gz
	SRR33252932_1.fastq.gz	Fastqsanger.gz
	SRR33252932_2.fastq.gz	Fastqsanger.gz
	SRR33252933_1.fastq.gz	Fastqsanger.gz

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KSHV Reprograms Host RNA Splicing via FAM50A to Activate STAT3 and Drive Oncogenic Cellular Transformation

Project description:RNA alternative splicing is a fundamental cellular process implicated in cancer development. Kaposi’s sarcoma-associated herpesvirus (KSHV), the etiological agent of multiple human malignancies, including Kaposi’s sarcoma (KS), remains a significant concern, particularly in AIDS patients. A CRISPR-Cas9 screening of matched primary rat mesenchymal stem cells (MM) and KSHV-transformed MM cells (KMM) identified key splicing factors involved in KSHV-induced cellular transformation. To elucidate the mechanisms by which KSHV-driven splicing reprogramming mediates cellular transformation, we performed transcriptomic sequencing, identifying 131 differential alternative splicing transcripts, with exon skipping as the predominant event. Notably, these transcripts were enriched in vascular permeability, multiple metabolic pathways and ERK1/2 signaling cascades, which play key roles in KSHV-induced oncogenesis. Further analyses of cells infected with KSHV mutants lacking latent genes including vFLIP, vCyclin and viral miRNAs, as well as cells overexpressing LANA, revealed their involvement in alternative splicing regulation. Among the identified splicing factors, FAM50A, a component of the spliceosome complex C, was found to be crucial for KSHV-mediated transformation. FAM50A knockout resulted in distinct splicing profiles in both MM and KMM cells, and significantly inhibited KSHV-driven proliferation, cellular transformation and tumorigenesis. Mechanistically, FAM50A knockout altered SHP2 splicing, promoting an isoform with enhanced enzymatic activity that led to reduced STAT3 Y705 phosphorylation in KMM cells. These findings reveal a novel paradigm in which KSHV hijacks host splicing machinery, specifically FAM50A-mediated SHP2 splicing, to sustain STAT3 activation and drive oncogenic transformation.

2025-04-26 | GSE295315 | GEO

SERBP1 deacetylation inhibits ferroptosis to promote KSHV-induced cellular transformation by decaying lipoyltransferase 2 mRNA

Project description:Ferroptosis, a defensive strategy employed by the host to restrict pathogenic infections, has been implicated in the development and therapeutic responses of various types of tumors. However, the role of ferroptosis in KSHV-induced malignant tumors remains elusive. A steadily growing number of non-histone proteins have been identified as acetylation targets, their functions have yet to be revealed. In this study, we obtained a marked disparity in the landscape of acetylation between MM and KSHV-transformed MM (KMM) cells. SERBP1 deacetylation was upregulated in KMM cells and contributed to KSHV-induced cellular transformation by inhibiting ferroptosis. Mechanistically, KSHV-encoded viral interleukin-6 (vIL-6) hijacks SIRT3, a mitochondrial NAD+-dependent deacetylase, to interact with SERBP1 leading to the deacetylation of SERBP1. Deacetylated SERBP1 exhibits reduced binding to Lipt2 mRNA, which promotes Lipt2 mRNA degradation, resulting in ferroptosis inhibition. Our findings unveil a novel role of SERBP1 deacetylation in regulating ferroptosis and KSHV-induced cellular transformation and identify potential new therapeutic targets for KSHV infection and KSHV-induced cancers.

2023-08-22 | GSE241111 | GEO

HOXA9 Reprograms the Enhancer Landscape During Leukemic Transformation

Project description:HOXA9 Reprograms the Enhancer Landscape During Leukemic Transformation

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Expression data in KSHV-infected primary rat mesenchymal precursor (MM) cells

Project description:Kaposi's sarcoma-associated herpesvirus (KSHV) can efficiently infect and transform primary rat mesenchymal precursor (MM) cells. Regulation of cell cycle progression and apoptosis by KSHV-encoded microRNAs is required for KSHV-induced cellular transformation and tumorigenesis. To determine the roles of KSHV miRs in growth deregulation, we infected MM cells with the KSHV miR cluster deletion mutant and monitored infection by examining green fluorescence protein expression from a cassette inserted in the KSHV genome.

2013-08-28 | E-GEOD-50381 | biostudies-arrayexpress

Expression data in KSHV-infected primary rat mesenchymal precursor (MM) cells

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KSHV regulation of gene expression in the human endothelial cell line EAHY

2011-11-29 | GSE33984 | GEO

KSHV regulation of gene expression in the human endothelial cell line EAHY

Project description:KSHV promotes endothelia to mesenchymal transformation (EntMT) in EAHY cells We have used Affymetrix Gene Arrays to investigate the patterns of regulation of gene expression in EAHY cells infected with KSHV in comparison to uninfected EAHY cells EAHY cells were infected with rKSHV.219 virus (derived from the virus-producing VERO cells). 12 days after infection and in puromycin selection to achieve greater than 90% infection RNA was exctrated from KSHV infected and control non-infected cells.

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YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (ChIP-seq)

Project description:The YAP and TAZ paralogues, the ultimate effectors of the Hippo signaling pathway, are deregulated in many cancer types. They are transcriptional co-activators that are recruited to their target sites, primarily by TEAD proteins. Here, we show that YAP and TAZ are also recruited by JUNB and STAT3, key factors that mediate an epigenetic switch linking inflammation to breast cellular transformation. YAP and TAZ directly interact with JUNB and STAT3 via a WW domain that is important for transformation, co-occupy many target sites in vivo via the sequence motifs of AP-1 and (to a lesser extent) STAT3, and stimulate transcriptional activation by AP-1 proteins. A small minority of target sites are YAP- or TAZ-specific, and they are associated with different sequence motifs and gene classes. YAP/TAZ, JUNB, and STAT3 directly regulate a common set of target genes that overlap, but are distinct from, those regulated by YAP/TAZ and TEADs. The set of target genes regulated by YAP/TAZ, STAT3, and JUNB is associated with poor survival in breast cancer patients with the triple-negative form of the disease.

2021-02-18 | GSE166941 | GEO

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation (RNA-seq)

2021-02-18 | GSE166942 | GEO

ac4C-seq of cellular and KSHV transcripts in iSLK-Puro, iSLK-KSHV (i.e. iSLK-RGB), iSLK-KSHV (WT), iSLK-KSHV (ΔNAT10) cells

Project description:We used ac4C-seq to detedc cellular and KSHV transcripts in iSLK-Puro, iSLK-KSHV, iSLK-KSHV (WT), iSLK-KSHV (ΔNAT10) cells after after doxycycline and sodium butyrate treatment.

2023-09-27 | GSE174161 | GEO

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