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Aberrant induction of the rare RNA binding protein PABPC4 in MYC-driven hepatocellular carcinoma [RIP-seq]

ABSTRACT: Aberrant induction of the rare RNA binding protein PABPC4 in MYC-driven hepatocellular carcinoma [RIP-seq]

PROVIDER: PRJNA977638 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24763823_1.fastq.gz	Fastqsanger.gz
	SRR24763823_2.fastq.gz	Fastqsanger.gz
	SRR24763824_1.fastq.gz	Fastqsanger.gz
	SRR24763824_2.fastq.gz	Fastqsanger.gz
	SRR24763825_1.fastq.gz	Fastqsanger.gz

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Aberrant induction of the rare RNA binding protein PABPC4 in MYC-driven hepatocellular carcinoma [RIP-seq]

Project description:PABPC4 is a member of the poly(A)-binding protein (PABP) family, responsible for regulating post-transcriptional gene expression. While PABPC1 is widely expressed and has a general function in translation initiation and mRNA stability, PABPC4 shows lower expression levels and a more tissue-specific pattern. It plays a role in specific biological processes such as erythroid differentiation and oogenesis. The precise regulation and specific role of PABPC4 in hepatocellular carcinoma (HCC) have remained unclear despite previous studies highlighting its involvement in HCC cell lines. To uncover potential downstream targets of PABPC4 in HCC cells, we conducted RNA-seq and RIP-seq analyses to identify mRNAs that were both downregulated in PABPC4-deficient cells and bound by PABPC4.

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Aberrant induction of the rare RNA binding protein PABPC4 in MYC-driven hepatocellular carcinoma [RNA-seq]

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Aberrant induction of the rare RNA binding protein PABPC4 in MYC-driven hepatocellular carcinoma

Project description:Aberrant induction of the rare RNA binding protein PABPC4 in MYC-driven hepatocellular carcinoma

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Aberrant induction of the rare RNA binding protein PABPC4 in MYC-driven hepatocellular carcinoma

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The role of HNRNPC-PABPC4 on polyA site selection

Project description:Cancer cells often co-opt post-transcriptional regulatory mechanisms to achieve pathologic expression of gene networks that drive metastasis. Translational control is a major regulatory hub in oncogenesis, however its effects on cancer progression remain poorly understood. To address this, we used ribosome profiling to compare genome-wide translation efficiencies of poorly and highly metastatic breast cancer cells and patient-derived xenografts. We developed novel regression-based methods to analyze ribosome profiling and alternative polyadenylation data, and identified HNRNPC as a translational controller of a specific mRNA regulon. Mechanistically, HNRNPC, in concert with PABPC4, binds near to poly(A) signals, thereby governing the alternative polyadenylation of a set of mRNAs. We found that HNRNPC and PABPC4 are downregulated in highly metastatic cells, which causes HNRNPC-bound mRNAs to undergo 3’ UTR lengthening and subsequently, translational repression. We showed that modulating HNRNPC expression impacts the metastatic capacity of breast cancer cells in xenograft mouse models. We also found that a small molecule, previously shown to induce a distal-to-proximal poly(A) site switching, counteracts the HNRNPC-PABPC4 driven deregulation of alternative polyadenylation and decreases the metastatic lung colonization by breast cancer cells in vivo.

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