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Syntaphilin regulates neutrophil migration in cancer

ABSTRACT: Syntaphilin regulates neutrophil migration in cancer

PROVIDER: PRJNA787303 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17173163.fastq.gz	Fastqsanger.gz
	SRR17173164.fastq.gz	Fastqsanger.gz
	SRR17173165.fastq.gz	Fastqsanger.gz
	SRR17173166.fastq.gz	Fastqsanger.gz
	SRR17173167.fastq.gz	Fastqsanger.gz

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Syntaphilin regulates neutrophil migration in cancer

Project description:Pathologically activated neutrophils (PMN) with immune suppressive activity - myeloid-derived suppressor cells (PMN-MDSC) - play a critical role in regulation of tumor progression. They were implicated in promotion of tumor metastases by contributing to pre-metastatic niche formation. This effect was facilitated by enhanced spontaneous migration of PMN in early stage cancers. The molecular mechanisms underpinning this phenomenon remained unclear. We found that syntaphilin (SNPH), a cytoskeletal protein previously known for anchoring mitochondria to the microtubule in neurons and tumor cells, could regulate migration of PMN. Expression of SNPH was decreased in PMN from tumor bearing mice and cancer patients as compared to PMN from tumor-free mice and healthy donors, respectively. Deletion of SNPH increased spontaneous migration of PMN and promoted tumor metastasis. Mechanistically, deletion of SNPH increased the speed and distance travelled by mitochondria, elevated rates of oxidative phosphorylation and glycolysis, and increased generation of adenosine. Thus, our study reveals a molecular mechanism regulating increased migratory activity of PMN during cancer progression and suggests novel targeting opportunity.

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Project description:Tumor-associated neutrophils are found in many types of cancer and are often reported to contribute to negative outcomes. Several studies have shown that the presence of TGF-β in the tumor microenvironment contributes to the skewing of neutrophils to have a more pro-tumor phenotype. However, the direct effects of TGF-β on neutrophil signaling and migration are unclear. We sought to characterize TGF-β signaling in both primary human neutrophils and the neutrophil-like cell line HL-60 and determine whether TGF-β directly induces neutrophil migration. We found that TGF-β1 does not induce neutrophil migration in either a transwell or an underagarose migration assay. However, TGF-β1 does activate signals canonically through SMAD3 and noncanonically through ERK1/2 in neutrophils in a time and dose-dependent manner. Additionally, TGF-β1 present in the tumor-conditioned media (TCM) is responsible for SMAD3 activation. Moreover, we discovered that TCM from aggressive breast cancer cells induces neutrophils to secrete leukotriene B4 (LTB4), which is a lipid mediator important for amplifying neutrophil recruitment. However, we found that TGF-β1 alone does not induce secretion of LTB4. We next performed RNA-sequencing to evaluate the effects of TGF-β1 and TCM on the neutrophil transcriptome. We found that TGF-β1 and TCM result in changes in gene transcription in HL-60 cells, specifically of two pro-tumor genes OSM and VEGFA. Together, our findings characterize the effects of TGF-β1 on neutrophil signaling, migration, and gene expression that can be applied to understanding the changes in neutrophils that occur in the tumor microenvironment.

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