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Phase separation of RXRγ drives tumor chemoresistance and represents a therapeutic target for small cell lung cancer

ABSTRACT: Phase separation of RXRγ drives tumor chemoresistance and represents a therapeutic target for small cell lung cancer

PROVIDER: PRJNA1163714 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30758487.fastq.gz	Fastqsanger.gz
	SRR30758488.fastq.gz	Fastqsanger.gz
	SRR30758489.fastq.gz	Fastqsanger.gz
	SRR30758490.fastq.gz	Fastqsanger.gz
	SRR30758491.fastq.gz	Fastqsanger.gz

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Phase separation of RXRγ drives tumor chemoresistance and represents a therapeutic target for small cell lung cancer

Project description:Phase separation of RXRγ drives tumor chemoresistance and represents a therapeutic target for small cell lung cancer

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Phase separation of RXRγ drives tumor chemoresistance and represents a therapeutic target for small cell lung cancer

Project description:Small cell lung cancer (SCLC) is the most lethal type of lung cancer, characterized by limited treatment options and rapid evolution from chemosensitivity to chemoresistance. However, the mechanisms underlying this evolution remain poorly understood. Identifying the druggable drivers and developing pharmacological strategies to overcome chemoresistance are imperative. Here, we show that Retinoid X receptor γ (RXRγ) is uniquely overexpressed in chemo-resistant SCLC tumors, and that RXRγ serves as an essential factor driving chemoresistance in SCLC. RXRγ forms phase-separated droplets with LSD1 in the nucleus, which enhances RXRγ-mediated gene transcription activity and reprograms gene expression, promoting tumor stemness and metastasis, and eventually driving SCLC chemoresistance. In turn, RXRγ antagonist disrupts RXRγ-LSD1 interaction, reducing their binding to the target gene locus, markedly suppressing the expression of the RXRγ target gene network. Finally, RXRγ antagonists strongly suppress tumor growth and metastasis and restore SCLC vulnerability to chemotherapy in multiple preclinical SCLC models, without overt toxicity, in mice. Thus, these results establish RXRγ as a key player in SCLC by phase separation and as a potential therapeutic target for this deadly disease.

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Project description:Chromosome translocation is known to generate oncogenes such as SS18-SSX1, but the underlying mechanism remains unknown. Here we show that enhanced phase separation acquired by translocation mediates oncogenic transformation. SSX fusion dramatically enhances the phase separation property of SS18 protein through H2AK119ub. Super condensates generated by SS18-SSX recruit acetyltransferases CBP/P300 as wild type SS18, but exclude HDACs such that H3K27ac accumulates abnormally at loci from those normally occupied by SS18, resulting aberrant silencing and activation of target genes. Consistently, we show that inhibition of H3K27ac can attenuate the tumorigenicity of the fusion oncoprotein. These results provide the first case for phase separation as a transforming event to generate oncogene and super phase separation can be targeted for cancer therapy.

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