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RNA-seq of Splenic CD4+ T cells and colon epithelial cells from miR-34a-/- and wildtype mice

ABSTRACT: RNA-seq of Splenic CD4+ T cells and colon epithelial cells from miR-34a-/- and wildtype mice

PROVIDER: PRJNA509684 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8314870.fastq.gz	Fastqsanger.gz
	SRR8314871.fastq.gz	Fastqsanger.gz
	SRR8314862.fastq.gz	Fastqsanger.gz
	SRR8314872.fastq.gz	Fastqsanger.gz
	SRR8314863.fastq.gz	Fastqsanger.gz

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RNA-seq of Splenic CD4+ T cells and colon epithelial cells from miR-34a-/- and wildtype mice

Project description:miR-34a is a known tumor suppressor that targets cell proliferation and apoptosis genes. In this study, we have shown that miR-34a acts as a safeguard for the inflammatory stem cell niche and reparative regeneration by modulating both the immune and epithelial responses to infection and inflammation. We isolated CD4+ T cells and colon epithelial cells from miR-34a-/- and wildtype mice revealed various changes in gene expression.

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Identification of SART3 as a pre-miR-34a–binding protein

Project description:MicroRNAs (miRNAs or miRs) are small, noncoding RNAs that are implicated in the regulation of nearly all biological processes. Global miRNA biogenesis is altered in many cancers and RNA-binding proteins (RBPs) have been shown to play a role in this process, presenting a promising avenue for targeting miRNA dysregulation in disease. miR-34a exhibits tumor-suppressive functions by targeting cell cycle regulators CDK4/6 and anti-apoptotic factor Bcl-2, among other regulatory pathways such as Wnt, TGF-, and Notch signaling. Many cancers show downregulation or loss of miR-34a, and synthetic miR-34a supplementation has been shown to inhibit tumor growth in vivo; however, the post-transcriptional mechanisms by which miR-34a is lost in cancer are not entirely understood. Here, we have used a proteomics-mediated approach to identify Squamous cell carcinoma antigen recognized by T-cells 3 (SART3) as a putative pre-miR-34a-binding protein. SART3 is a spliceosome recycling factor and nuclear RBP with no previously reported role in miRNA regulation. We demonstrate that SART3 binds pre-miR-34a with specificity over pre-let-7d and begin to elucidate a new functional role for this protein in non-small lung cancer cells. Overexpression of SART3 led to increased miR-34a levels, downregulation of the miR-34a target genes CDK4 and CDK6, and cell cycle arrest in the G1 phase. In vitro binding studies showed that the RNA-recognition motifs within the SART3 sequence are responsible for selective pre-miR-34a binding. Collectively, our results present evidence for an influential role of SART3 in miR-34a biogenesis and cell cycle progression.

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