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Role for citron kinase in prostate cancer growth

ABSTRACT: Role for citron kinase in prostate cancer growth

PROVIDER: PRJNA510399 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR8330960_1.fastq.gz	Fastqsanger.gz
	SRR8330960_2.fastq.gz	Fastqsanger.gz
	SRR8330961_1.fastq.gz	Fastqsanger.gz
	SRR8330961_2.fastq.gz	Fastqsanger.gz
	SRR8330952_1.fastq.gz	Fastqsanger.gz

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Role for citron kinase in prostate cancer growth

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Chemokine receptor CXCR7 activates Aurora Kinase A and promotes neuroendocrine prostate cancer growth

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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.

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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]

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RET Kinase Inhibition in Neuroendocrine Prostate Cancer, part 1

Project description:Increased treatment of metastatic castration resistant prostate cancer (mCRPC) with second-generation anti-androgen therapies (ADT) has coincided with a greater incidence of lethal, aggressive variant prostate cancer (AVPC) tumors that have lost androgen receptor (AR) signaling. AVPC tumors may also express neuroendocrine markers, termed neuroendocrine prostate cancer (NEPC). Recent evidence suggests kinase signaling may be an important driver of NEPC. To identify targetable kinases in NEPC, we performed global phosphoproteomics comparing AR-negative to AR-positive prostate cancer cell lines and identified multiple altered signaling pathways, including enrichment of RET kinase activity in the AR-negative cell lines. Clinical NEPC and NEPC patient derived xenografts displayed upregulated RET transcript and RET pathway activity. Pharmacologically inhibiting RET kinase in NEPC models dramatically reduced tumor growth and cell viability in mouse and human NEPC models. Our results suggest that targeting RET in NEPC tumors with high RET expression may be a novel treatment option.

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RET Kinase Inhibition in Neuroendocrine Prostate Cancer, part 2

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A role for the mitogen-activated protein kinase kinase kinase 1 in epithelial wound healing

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HPK-1 Citron Homology Domain interactions with Kinase Domain

Project description:The files uploaded here are converted into a standard mzxml format, and utilize processing procedures described in 10.1021/acs.analchem.9b01682 Briefly, HXMS data processing consists of 1. MSMS experiment to identify peptides and their associated retention times. These files have *MSMS* in the filename. They are searched using HPK.fasta. 2. Unlabeled peptide pool file is used to refine the exact RT range of the peptide in the experiment (MSMS experiment may be conducted at a different time). 3. Labeling experiments are then searched using ExMS2 (see manuscript linked above) to produce carried deuterium at each time point for peptides included in the pool. Comparing uptake patterns between "FullLength" files and "Kinase" files produces the map of differences on the kinase domain induced by the citron homology domain. There are two CSV files, these contain the peptides identified in each MSMS run. These are found in Search Engine Files. There are also finaltables produced by the ExMS program containing all raw and unfiltered results. There is a pdf file associated that shows the final peptides used for the analyses after discarding noisy peptides upon manual inspection. All protection factors extracted from this data along with a summary table can be found in "File_HX_TABLES.xlsx".

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