Genomics,Multiomics

Dataset Information

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RNAseq data comparing KRAS*-independent HDAC5 eccaper PDAC cells and KRAS*-dependent iKPC PDAC cells


ABSTRACT: HDAC5 drives PDAC cells to bypass KRAS* dependency. To dissect the molecular mechanisms that regulated by overexpressed HDAC5 in the bypass of KRAS* dependency, we conducted RNA-seq analysis of HDAC5 escaper PDAC cells and KRAS*-expressing iKPC PDAC cells. Overall design: Four KRAS* expressing iKPC PDAC cell lines and five HDAC5 escaper PDAC cell lines were used.

INSTRUMENT(S): Illumina HiSeq 2000 (Mus musculus)

ORGANISM(S): Mus Musculus

SUBMITTER: Pingping Hou  

PROVIDER: GSE149126 | GEO | 2020-04-27

REPOSITORIES: GEO

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Publications


Oncogenic KRAS (KRAS*) is a key tumor maintenance gene in pancreatic ductal adenocarcinoma (PDAC), motivating pharmacologic targeting of KRAS* and its effectors. Here, we explored mechanisms involving the tumor microenvironment (TME) as a potential basis for resistance to targeting KRAS*. Using the inducible <i>Kras</i> <sup>G12D</sup>;<i>Trp53</i> <sup>-/-</sup> PDAC mouse model, gain-of-function screens of epigenetic regulators identified <i>HDAC5</i> as the top hit enabling KRAS* independent  ...[more]

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