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Global gene targets of PIM kinases in human Th17 cells

ABSTRACT: Global gene targets of PIM kinases in human Th17 cells

PROVIDER: PRJNA967238 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24434400_1.fastq.gz	Fastqsanger.gz
	SRR24434400_2.fastq.gz	Fastqsanger.gz
	SRR24434401_1.fastq.gz	Fastqsanger.gz
	SRR24434401_2.fastq.gz	Fastqsanger.gz
	SRR24434402_1.fastq.gz	Fastqsanger.gz

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Bulk RNA sequencing of PIM-silenced human Th17 cells

Project description:The aim of this study was to investigate the transciptional mechanisms regulated by three PIM kinases during early human Th17 cell differentiation. PIM kinases were transiently silenced using RNAi (KD) approach followed by RNA-seq to determine their global transciptional targets.

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Single cell RNA sequencing of PIM-silenced human Th17 cells

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Transcriptome analysis PIM kinase inhibition vs degradation

Project description:PIM kinases have important pro-tumorigenic roles and mediate several oncogenic traits, including cell proliferation, survival, and chemotherapeutic resistance. As a result, multiple PIM inhibitors have been pursued as investigational new drugs in cancer; however, response to PIM inhibitors in solid tumors has fallen short of expectations. We found that inhibition of PIM kinase activity stabilizes protein levels of all three PIM isoforms (PIM1/2/3), and this can promote resistance to PIM inhibitors and chemotherapy. To overcome this effect, we designed PIM proteolysis targeting chimeras (PROTACs) to target PIM for degradation. PIM PROTACs effectively downmodulated PIM levels through the ubiquitin-proteasome pathway. Importantly, degradation of PIM kinases was more potent than inhibition of catalytic activity in inducing apoptosis in prostate cancer cell line models. In conclusion, we provide evidence of the advantages of degrading PIM kinases versus inhibiting their catalytic activity to target the oncogenic functions of PIM kinases.

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Global gene targets of PIM kinases in human Th17 cells

Project description:This SuperSeries is composed of the SubSeries listed below.

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Bulk RNA sequencing of PIM-silenced human Th17 cells

Project description:Bulk RNA sequencing of PIM-silenced human Th17 cells

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Project description:The serine/threonine-specific Moloney murine leukemia virus (PIM) kinase family (i.e., PIM1, PIM2, and PIM3) has been extensively studied in tumorigenesis. PIM kinases are downstream of several cytokine signaling pathways that drive immune-mediated diseases. Uncontrolled T helper 17 (Th17) cell activation has been associated with the pathogenesis of autoimmunity. However, the detailed molecular function of PIMs in human Th17 cell regulation has yet to be studied. In the present study, we comprehensively investigated how the three PIMs simultaneously alter transcriptional gene regulation during early human Th17 cell differentiation. By combining PIM triple knockdown with bulk and scRNA-seq approaches, we found that PIM deficiency promotes the early expression of key Th17-related genes while suppressing Th1-lineage genes. Further, PIMs modulate Th cell signaling, potentially via STAT1 and STAT3. Overall, our study highlights the inhibitory role of PIMs in human Th17 cell differentiation, thereby suggesting their association with autoimmune phenotypes.

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