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Cancer cells educate natural killer cells to a metastasis-promoting cell state

ABSTRACT: Cancer cells educate natural killer cells to a metastasis-promoting cell state

PROVIDER: PRJNA640407 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12047073.fastq.gz	Fastqsanger.gz
	SRR12047073_1.fastq.gz	Fastqsanger.gz
	SRR12047073_2.fastq.gz	Fastqsanger.gz
	SRR12047074.fastq.gz	Fastqsanger.gz
	SRR12047074_1.fastq.gz	Fastqsanger.gz

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Cancer cells educate natural killer cells to a metastasis-promoting cell state.

Project description:Natural killer (NK) cells have potent antitumor and antimetastatic activity. It is incompletely understood how cancer cells escape NK cell surveillance. Using ex vivo and in vivo models of metastasis, we establish that keratin-14+ breast cancer cells are vulnerable to NK cells. We then discovered that exposure to cancer cells causes NK cells to lose their cytotoxic ability and promote metastatic outgrowth. Gene expression comparisons revealed that healthy NK cells have an active NK cell molecular phenotype, whereas tumor-exposed (teNK) cells resemble resting NK cells. Receptor-ligand analysis between teNK cells and tumor cells revealed multiple potential targets. We next showed that treatment with antibodies targeting TIGIT, antibodies targeting KLRG1, or small-molecule inhibitors of DNA methyltransferases (DMNT) each reduced colony formation. Combinations of DNMT inhibitors with anti-TIGIT or anti-KLRG1 antibodies further reduced metastatic potential. We propose that NK-directed therapies targeting these pathways would be effective in the adjuvant setting to prevent metastatic recurrence.

| S-EPMC7480097 | biostudies-literature

Cancer cells educate natural killer cells to a metastasis-promoting cell state

Project description:Gene expression comparisons revealed that healthy NK cells have an active NK cell molecular phenotype, whereas tumor-exposed (teNK) cells resemble resting NK cells. Receptor–ligand analysis between teNK cells and tumor cells revealed multiple potential targets.

2020-06-25 | GSE152790 | GEO

Expression profiling of Natural killer B cells

Project description:Investigation of global gene expression levels between B cells, Natural killer cells and Natural killer B cells Gene expression profiling using sorted B cells, Natural killer cells and Natural killer B cells from WT mouse spleen. Total RNA extracted from WT cells were quantified by the NanoDrop ND-1000 and RNA integrity was assessed by standard denaturing agarose gel electrophoresis. The sample preparation and microarray hybridization were performed based on the NimbleGenâs standard protocols.

2016-05-17 | E-GEOD-80063 | biostudies-arrayexpress

Natural killer cells promote fetal development through the secretion of growth-promoting factors

Project description:Natural killer (NK) cells are present in large populations at the maternal-fetal interface during early pregnancy, but their roles in fetal growth are unclear. Here, we identify a CD49a+Eomes+ subset of NK cells that have the capability to secrete growth-promoting-factors (GPF), including pleiotrophin, osteoglycin and osteopontin in both humans and mice. Decreases in this GPF-secreting NK subset impair fetal development, and leads to fetal growth restriction. The transcriptional factor Nfil3 but not T-bet affects the function and the number of this decidual NK subset. The crosstalk of the HLA-G-ILT2-KIR2DL4 axis promotes the GPF-secreting function of this NK subset. Adoptive transfer of these induced CD49a+Eomes+NK cells can reverse the impaired fetal growth and rebuild an appropriate local microenvironment. These findings reveal new properties of NK cells in promoting fetal growth as well as novel approaches for therapeutically administering NK cells to reverse restricted nourishments within the microenvironment during early pregnancy. To investigate novel molecular signatures of human decidual NK cells, we performed microarray analysis on dNK cells (CD3−CD56+CD49a+CD49b−) and pNK cells (CD3−CD56+CD49a−CD49b+). dNK cells were purified from first-trimester deciduas. pNK cells were purified from adult peripheral blood mononuclear cells. Samples were collected from healthy adult donors after obtaining informed consent according to the Ethics Committee of the University of Science & Technology of China.

2018-01-04 | GSE97217 | GEO

Expression profiling of Natural killer B cells

Project description:Investigation of global gene expression levels between B cells, Natural killer cells and Natural killer B cells

2016-05-17 | GSE80063 | GEO

Transcription profiling of neonatal and adult mouse natural killer cells

Project description:Comparing global gene expression of neonatal and adult natural killer cells to determine if differences in gene expression suggest that different developmental pathways during hematopoiesis are followed in the fetal and adult mouse to produce mature natural killer cells.

2005-10-01 | E-MEXP-354 | biostudies-arrayexpress

RUNX2-specific human Natural Killer (NK) cells

Project description:RUNX2-specific human Natural Killer (NK) cells

| PRJNA723303 | ENA

Efficacy and safety of Natural Killer cells injection combined with XELOX chemotherapy for postoperative colorectal cancer patients

Project description:Interventions: Treatment Group:Natural Killer cells injection;Control Group:sodium chloride injection Primary outcome(s): overall survival, progression-free survival;SafetyEvaluation Study Design: Parallel

| 113367 | ecrin-mdr-crc

Regulation of natural killer cells during MCMV infection

Project description:Regulation of natural killer cells during MCMV infection

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The transcription factor PBX1 drives natural killer cells to promote fetal development

Project description:Perfect fetal development is a solid foundation for successful fertility, in which the abundant natural killer (NK) cells in the decidua tissue at the maternal-fetal interface play an important role during the first trimester. The functional subsets and transcriptional regulation mechanisms of decidual NK (dNK) cells remain poorly understood. Here, we identified CD49a+PBX1+ dNK cells as a unique subset of NK cells that promote fetal development in both human and mice. PBX1 drove the transcription of key functional molecules pleiotrophin and osteoglycin that promote fetal development through direct promoter binding. In patients with unexplained recurrent spontaneous abortion (URSA), decreased expression of PBX1 and PBX1(G21S) mutation correlated with fetal growth restriction and pregnancy failure. Inactivation of Pbx1 in mouse NK cells caused impaired fetal development due to a decrease in growth promoting factors. Our observations reveal the molecular regulation mechanism of CD49a+PBX1+ dNK cells promoting fetal development, and indicate that impaired PBX1 in dNK cells may serve as pathogenesis and biomarker of URSA.

2021-01-01 | GSE110244 | GEO

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