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Transcriptional response to PORCN inhibition using an in vivo model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II) in EP300 knockout and WT cells

ABSTRACT: Transcriptional response to PORCN inhibition using an in vivo model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II) in EP300 knockout and WT cells

PROVIDER: PRJNA762294 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15838066_1.fastq.gz	Fastqsanger.gz
	SRR15838066_2.fastq.gz	Fastqsanger.gz
	SRR15838067_1.fastq.gz	Fastqsanger.gz
	SRR15838067_2.fastq.gz	Fastqsanger.gz
	SRR15838068_1.fastq.gz	Fastqsanger.gz

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Transcriptional response to PORCN inhibition using an in vivo model of RNF43 mutant pancreatic adenocarcinoma (HPAF-II) in EP300 knockout and WT cells

Project description:RNF43-mutant pancreatic tumors are driven by Wnt signaling and sensitive to Wnt inhibition, e.g. PORCN inhibitors. However, some RNF43-mutant pancreatic cancers are intrinsically resistant to Wnt inhibition. We identified that EP300 mutations confer resistance to PORCN inhibitors in RNF43-mutant pancreatic cancers. We found that EP300 knockout down-regulated GATA6 expression and GATA6-regulated differentiation program, making the anti-differentiation roles of Wnt signaling dispensable.

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Project description:It has been demonstrated that Ring finger protein 43 (RNF43) is overexpressed in colorectal cancer and mediates cancer cell proliferation. We found that RNF43 was frequently overexpressed in HCC, and knockdown of RNF43 could induce apoptosis and inhibit proliferation, invasion, colony formation and xenograft growth of HCC cells. Suggesting that RNF43 is involved in tumorigenesis and progression of HCC. We used microarrays to profile gene expression patterns before and after RNF43 knockdown, and identified differentially expressed genes during this process. HepG2 cells were transfected with RNF43 siRNA or negative control siRNA in triplicate. Forty-eight hours after transfection, total RNA was extracted,labeled and hybridized to HG-U133 Plus 2.0 arrays.

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