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ATF6 is required for the survival of castration-resistant prostate cancer cells

ABSTRACT: ATF6 is required for the survival of castration-resistant prostate cancer cells

PROVIDER: PRJNA818029 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18391012.fastq.gz	Fastqsanger.gz
	SRR18391013.fastq.gz	Fastqsanger.gz
	SRR18391014.fastq.gz	Fastqsanger.gz
	SRR18391015.fastq.gz	Fastqsanger.gz
	SRR18391016.fastq.gz	Fastqsanger.gz

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ATF6 is required for the survival of castration-resistant prostate cancer cells

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Project description:Resistance to androgen deprivation therapies and increased androgen receptor (AR) activity are major drivers of castration-resistant prostate cancer (CRPC). Prior work has focused on targeting AR directly; however, the identification and targeting of co-activators of AR signaling remains an underexplored area. Here we demonstrate that the MLL (mixed-lineage leukemia) complex, a well-known contributor in MLL-fusion-positive leukemia, acts as a co-activator of AR signaling. AR interacts with the MLL complex via its subunit, menin. Small molecule inhibition of the menin-MLL interaction blocks AR signaling and inhibits tumor growth in vivo. Furthermore, we find that menin is up-regulated in CRPC and high expression correlates with poor overall survival. Our study identifies the MLL complex as a co-activator of AR that can be targeted in advanced prostate cancer. ASH2L / Menin / MLL1 were knocked down using shRNA /siRNA in two prostate cancer cell lines, VCaP and LNCaP.

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