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PRPF19 Inhibition Attenuates Non-Small Cell Lung Cancer Progression through Impairing Citron Kinase-controlled Cytokinesis and Enhancing Anti-tumor Immune Responses [Prpf19_KP-1_RNAseq]

ABSTRACT: PRPF19 Inhibition Attenuates Non-Small Cell Lung Cancer Progression through Impairing Citron Kinase-controlled Cytokinesis and Enhancing Anti-tumor Immune Responses [Prpf19_KP-1_RNAseq]

PROVIDER: PRJNA1081288 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28115336_1.fastq.gz	Fastqsanger.gz
	SRR28115336_2.fastq.gz	Fastqsanger.gz
	SRR28115337_1.fastq.gz	Fastqsanger.gz
	SRR28115337_2.fastq.gz	Fastqsanger.gz
	SRR28115338_1.fastq.gz	Fastqsanger.gz

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PRPF19 Inhibition Attenuates Non-Small Cell Lung Cancer Progression through Impairing Citron Kinase-controlled Cytokinesis and Enhancing Anti-tumor Immune Responses [PRPF19_H2009_RNAseq]

Project description:Non-small cell lung cancer (NSCLC) remains the leading cause of cancer-related death, primarily due to limited therapeutic targets and the emergence of drug resistance. In this study, we conducted CRISPR knockout screens to identify the pre-mRNA processing factor 19 (PRPF19) as a potential therapeutic target for NSCLC. Our findings revealed that PRPF19 is highly expressed in NSCLC, and its expression is negatively correlated with the clinical outcomes. Through functional validation, we confirmed that genetic ablation of PRPF19 significantly attenuated cancer progression both in vitro and in vivo. Mechanistically, we discovered that PRPF19 plays a crucial role in regulating the precise location of Citron Kinase (CIT) within the contractile ring, thereby sustaining the normal cytokinesis processes. Inhibition of PRPF19 resulted in cytokinesis failure, leading to micronuclei formation and activating the anti-tumor immune response through the TBK1-IFNs pathway. Taken together, our results demonstrate the critical involvement of the PRPF19-CIT axis in NSCLC progression and suggest that targeting PRPF19 represents a promising therapeutic approach for NSCLC patients.

2024-03-03 | GSE259344 | GEO

PRPF19 Inhibition Attenuates Non-Small Cell Lung Cancer Progression through Impairing Citron Kinase-controlled Cytokinesis and Enhancing Anti-tumor Immune Responses [Prpf19_KP-1_RNAseq]

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PRPF19 Inhibition Attenuates Non-Small Cell Lung Cancer Progression through Impairing Citron Kinase-controlled Cytokinesis and Enhancing Anti-tumor Immune Responses [PRPF19_H2009_RNAseq]

Project description:PRPF19 Inhibition Attenuates Non-Small Cell Lung Cancer Progression through Impairing Citron Kinase-controlled Cytokinesis and Enhancing Anti-tumor Immune Responses [PRPF19_H2009_RNAseq]

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Org.one project - Citron-Crested Cockatoo

Project description:Org.one project - Citron-Crested Cockatoo

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Role for citron kinase in prostate cancer growth

Project description:Role for citron kinase in prostate cancer growth

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p27(Kip1) controls cytokinesis via the regulation of citron kinase activation.

Project description:p27(Kip1) (p27) acts as a tumor suppressor by inhibiting cyclin-cyclin-dependent kinase (cyclin-CDK) activity. However, mice expressing a form of p27 that is unable to bind or inhibit cyclin-CDK complexes (p27(CK-)) have increased incidence of tumor development as compared with wild-type and p27(-/-) mice, revealing an oncogenic role for p27. Here, we identified a phenotype of multinucleation and polyploidy in p27(CK-) mice not present in p27(-/-) animals, suggesting a role for p27 in G2/M that is independent of cyclin-CDK regulation. Further analysis revealed that p27(CK-) expression caused a cytokinesis and abscission defect in mouse embryonic fibroblasts. We identified the Rho effector citron kinase (citron-K) as a p27-interacting protein in vitro and in vivo and found that p27 and citron-K colocalized at the contractile ring and mid-body during telophase and cytokinesis. Moreover, overexpression of the minimal p27-binding domain of citron-K was sufficient to rescue the phenotype caused by p27(CK-). Conversely, expression of a mutant p27(CK-) unable to bind citron-K did not induce multinucleation. Finally, by binding to citron-K, p27 prevented the interaction of citron-K with its activator RhoA. Taken together, these data suggest a role for p27 during cytokinesis via the regulation of citron-K activity.

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Project description:The mechanisms underlying completion of cytokinesis are still poorly understood. Here, we show that the Drosophila orthologue of mammalian Citron kinases is essential for the final events of the cytokinetic process. Flies bearing mutations in the Drosophila citron kinase (dck) gene were defective in both neuroblast and spermatocyte cytokinesis. In both cell types, early cytokinetic events such as central spindle assembly and contractile ring formation were completely normal. Moreover, cytokinetic rings constricted normally, leading to complete furrow ingression. However late telophases of both cell types displayed persistent midbodies associated with disorganized F actin and anillin structures. Similar defects were observed in dck RNA interference (RNAi) telophases, which, in addition to abnormal F actin and anillin rings, also displayed aberrant membrane protrusions at the cleavage site. Together, these results indicate that mutations in the dck gene result in morphologically abnormal intercellular bridges and in delayed resolution of these structures, suggesting that the wild-type function of dck is required for abscission at the end of cytokinesis. The phenotype of Dck-depleted cells is different from those observed in most Drosophila cytokinesis mutants but extraordinarily similar to that caused by anillin RNAi, suggesting that Dck and anillin are in the same pathway for completion of cytokinesis.

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Project description:Targeting lncRNA HUMT attenuates chemoresistance of LUAD via impairing glycolysis signaling

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Microarray analysis of Etrog citron (Citrus medica L.) reveals changes in chloroplast, cell wall, peroxidase and symporter activities in response to viroid infection

Project description:The main objective of the present study was to analyze the effect of a severe isolate of CEVd on gene expression of Etrog citron plants was performed not only in late (post-symptomatic) stages of infection but also in early (pre-symptomatic) stages. A genome-wide 20K cDNA mycroarray of citrus was used.

2012-11-01 | GSE28652 | GEO

Two-pore channel 1 interacts with citron kinase, regulating completion of cytokinesis.

Project description:Two-pore channels (TPC1, 2, and 3) are recently identified endolysosmal ion channels, but remain poorly characterized. In this study, we show for the first time a role for TPC1 in cytokinesis, the final step in cell division. HEK 293 T-REx cells inducibly overexpressing TPC1 demonstrated a lack of proliferation accompanied by multinucleation and an increase in G2/M cycling cells. Increased TPC1 was associated with a concomitant accumulation of active RhoGTP and a decrease in phosphorylated myosin light chain (MLC). Finally, we demonstrated a novel interaction between TPC1 and citron kinase (CIT). These results identify TPC1 as a central component of cytokinetic control, specifically during abscission, and introduce a means by which the endolysosomal system may play an active role in this process.

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