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BCL6 Enables Cancer Cells to Evade Genotoxic Stress

ABSTRACT: BCL6 Enables Cancer Cells to Evade Genotoxic Stress

PROVIDER: PRJNA679550 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13085030_1.fastq.gz	Fastqsanger.gz
	SRR13085030_2.fastq.gz	Fastqsanger.gz
	SRR13085031_1.fastq.gz	Fastqsanger.gz
	SRR13085031_2.fastq.gz	Fastqsanger.gz
	SRR13085032_1.fastq.gz	Fastqsanger.gz

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BCL6 Enables Cancer Cells to Evade Genotoxic Stress

Project description:Genotoxic agents remain the mainstay of cancer treatment. Unfortunately, clinical benefit is often countered by a rapid adaptive response in tumors. Here we report that the proto-oncogene BCL6 is a core component conferring tumor resistance adaption. In response to genotoxic stress, BCL6 transcription was markedly promoted in cancer cells. BCL6 upregulation was positively associated with therapy resistance and poor progression-free survival in patients. Mechanistically, we discovered that treatment of the genotoxic agent etoposide led to transcriptional reprogramming of multiple proinflammatory cytokines, among which interferon-α and interferon-γ response were significantly enriched in resistant cells. Our results further revealed that the interferon/STAT1 axis that was required for the therapeutic efficacy of etoposide directly regulated BCL6 expression. Increased BCL6 consequently activated mTOR pathway through repressing the tumor suppressor PTEN to enable cancer cell survival. Importantly, targeted inhibition of BCL6 potentiated etoposide-triggered DNA damage and apoptosis in vitro and in vivo. Collectively, our findings highlight the significance of targeting previously uncharacterized interferon-mediated BCL6 pathway to conquer tolerance of cancer cells to genotoxic stress.

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BCL6 evolved in vertebrates as a stress tolerance gene and is broadly used by cancer cells to adapt to stress

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