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Triple therapy reduced metastasis in triple-negative breast cancer.

ABSTRACT: Triple therapy reduced metastasis in triple-negative breast cancer.

PROVIDER: PRJNA832953 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18962139_1.fastq.gz	Fastqsanger.gz
	SRR18962139_2.fastq.gz	Fastqsanger.gz
	SRR18962140_1.fastq.gz	Fastqsanger.gz
	SRR18962140_2.fastq.gz	Fastqsanger.gz
	SRR18962141_1.fastq.gz	Fastqsanger.gz

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Triple therapy reduced metastasis in triple-negative breast cancer.

Project description:Purpose: To understand the underlying mechanisms of oncolytic virus therapy in breast cancer. Methods: The primary tumors of 4T1 in BALB/C mice were exstracted and analyzed by RNA-seq. Results: In consistent with previous studies, we found some anti-tumor factors were up-regulated. Interestingly, several immunosupressive genes were activited. Conclusion: Our study identified the intercellular and intracellular factors restricting the optimized oHSV efficacy and supported the rationally designed triple therapy for clinical translation.

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Project description:Triple-negative breast cancer (TNBC) has a relatively aggressive biological behavior and poor outcome. Our published study showed that PAI-1 could induce the migration and metastasis of TNBC cells. However, the underlying mechanism by which PAI-1 regulates TNBC metastasis has not been addressed. Using microarray analysis of lncRNA expression profiles, we identified a lncRNA SOX2-OT, which is by induced by PAI-1 and could function as an oncogenic lncRNA in TNBC.

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Flt3L therapy induces a Treg‐promoting cDC1 state in triple‐negative breast cancer

Project description:Conventional dendritic cells (cDCs) are at the forefront of activating the immune system to mount an anti‐tumor immune response. Flt3L is a cytokine required for DC development that can increase DC abundance in the tumor when administered therapeutically. However, the impact of Flt3L on the phenotype of distinct cDC subsets in the tumor microenvironment is still largely undetermined. Here, using multi‐omic single‐cell analysis, we show that Flt3L therapy increases all cDC subsets in orthotopic E0771 triple‐negative breast cancer, but this did not result in a reduction of tumor growth. Interestingly, a CD81+migcDC1 population, likely developing from cDC1, was induced upon Flt3L treatment. This subset is characterized by the expression of both canonical cDC1 markers as well as migratory cDC activation and regulatory markers and displayed a higher Treg‐inducing potential compared to other migcDCs. To shift the cDC phenotype towards a T‐cell stimulatory phenotype, CD40 agonist therapy was administered in combination with Flt3L. However, while αCD40 reduced tumor growth, Flt3L failed to improve the therapeutic response to αCD40 therapy. Interestingly, Flt3L+αCD40 combination therapy increased the abundance of Treg promoting CD81+migcDC1. Nonetheless, while Treg‐depletion and αCD40 therapy were synergistic, the addition of Flt3L to this combination did not result in any added benefit. Overall, these results indicate that merely increasing cDCs in the tumor by Flt3L treatment cannot improve anti‐tumor responses and therefore might not be beneficial for the treatment of triple‐negative breast cancer, though could still be of use to increase cDC numbers for autologous DC‐therapy.

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