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CDK5 activates Hippo signaling to confer resistance to radiotherapy via upregulating TAZ in lung cancer

ABSTRACT: CDK5 activates Hippo signaling to confer resistance to radiotherapy via upregulating TAZ in lung cancer

PROVIDER: PRJNA624894 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11539317.fastq.gz	Fastqsanger.gz
	SRR11539318.fastq.gz	Fastqsanger.gz
	SRR11539319.fastq.gz	Fastqsanger.gz
	SRR11539320.fastq.gz	Fastqsanger.gz
	SRR11539321.fastq.gz	Fastqsanger.gz

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CDK5 activates Hippo signaling to confer resistance to radiotherapy via upregulating TAZ in lung cancer

Project description:Tumor resistance to radiotherapy is a therapeutic challenge in the treatment of patients with lung cancer. Cyclin-dependent kinase 5 (CDK5) has been proposed to participate in cell proliferation, migration and invasion; drug resistance; and immune evasion. However, the functions and regulatory mechanisms of CDK5 in lung cancer radioresistance have not been investigated.SiRNAs and ShRNAs were used to knock down CDK5 in A549 and H1299 cells. The effects of CDK5 depletion on the tumorigenic behaviors of non-small cell lung cancer (NSCLC) cells were evaluated in vitro and in vivo. Gene expression was examined by RNA-seq and quantitative real-time PCR.

2021-04-30 | GSE148532 | GEO

Project description:CDK5 activates Hippo signaling to confer resistance to radiotherapy via upregulating TAZ in lung cancer.

| PRJNA622949 | ENA

Cdk5 drives formation of heterogeneous pancreatic neuroendocrine tumors.

Project description:Pancreatic neuroendocrine tumors (PanNETs) are a heterogeneous population of neoplasms that arise from hormone-secreting islet cells of the pancreas and have increased markedly in incidence over the past four decades. Non-functional PanNETs, which occur more frequently than hormone-secreting tumors, are often not diagnosed until later stages of tumor development and have poorer prognoses. Development of successful therapeutics for PanNETs has been slow, partially due to a lack of diverse animal models for pre-clinical testing. Here, we report development of an inducible, conditional mouse model of PanNETs by using a bitransgenic system for regulated expression of the aberrant activator of Cdk5, p25, specifically in b-islet cells. This model produces a heterogeneous population of PanNETs that includes a subgroup of well-differentiated, non-functional tumors. The utility of this model is enhanced by ability to form tumor-derived allografts. Production of these tumors demonstrates the causative potential of aberrantly active Cdk5 for generation of PanNETs. Further, we show that human PanNETs express Cdk5 pathway components, are dependent on Cdk5 for growth, and share genetic and transcriptional overlap with the INS-p25OE model. This new model of PanNETs will facilitate molecular delineation of Cdk5-dependent PanNETs and the development of new targeted therapeutics.

2021-06-10 | GSE176448 | GEO

CDK5-dependent phosphorylation and nuclear translocation of TRIM59 promotes macroH2A1 ubiquitination and tumorigenicity

Project description:Despite the development of adjuvant therapies, glioblastoma (GBM) patients remain incurable and justify the urgent need of new therapies. CDK5 functions a critical role in GBM and is a potential target for GBM. However, the mechanism by which CDK5 promotes GBM tumorigenicity remains largely unknown. Here we identify TRIM59 as a substrate of CDK5. EGFR-activated CDK5 directly binds to and phosphorylates TRIM59, a ubiquitin ligase at serine 308, which recruits PIN1 for cis-trans isomerization of TRIM59, leading to TRIM59 binding to importin a5 and nuclear translocation. Nuclear TRIM59 induces ubiquitination and degradation of the tumor suppressive histone variant macroH2A1, leading to enhanced STAT3 signaling activation and tumorigenicity. These findings are confirmed by inhibition of CDK5-activated TRIM59 activity that results in suppression of intracranial tumor growth. Correlative expressions of the components of this pathway are clinically prognostic. Our findings suggest targeting CDK5/TRIM59 signaling axis as a putative strategy for treating GBM.

2019-08-11 | GSE130949 | GEO

Cdk5 regulates activity-dependent gene expression and dendrite development [cultured cortical neurons]

Project description:To investigate the molecular mechanism underlying activity-dependent dendrite development regulated by Cdk5, an unbiased microarray analysis was performed to identify activity-dependent genes differentially regulated in cortical neurons from E18 Cdk5-knockout embryos.

2015-12-11 | GSE68320 | GEO

CDK5 inhibition abrogates TNBC stem-cell property and enhances anti-PD-1 therapy

Project description:Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer that shows high infiltration of cancer stem cells (CSCs), which correlates with poor clinical outcome. Here, we have demonstrated that an aberrant activation of CDK5/pho-PPARg axis associated with TNBC progression closely. CDK5 blockade sufficiently abrogates stemness transformation of TNBC cells, resulting in a significant inhibition of tumor metastatic progression. Moreover, CDK5 inhibitor Rosc attenuates CD44v+ BCSCs, hereby reversing immunosuppressive microenvironment and enhancing anti-PD-1 effects on TNBC. Mechanistically, CDK5/pho-PPARgaxis modulates the ESRP1 degradation via E3 ligase-like activity, leading to CD44 variant (CD44v) expression. Our finding indicates that CDK5 blockade could be a potent strategy to target CSCs in TNBC, and to increase the response to PD-1 blockade in TNBC therapy.

2022-06-18 | GSE132902 | GEO

Different gene expression between CDK5 knocking down and control colorectal cancer cell line HCT116

Project description:We sought to find out the molecular mechanism of CDK5 displayed in colorectal cancer. Microarray experiments were carried out to identify different gene expression between CDK5-knockdown HCT116 cell lines and Scramble HCT116 cell lines.

2016-05-05 | GSE81085 | GEO

CDK5-Cyclin B1 regulates mitotic progression and fidelity

Project description:Mammalian cell cycle is driven by several CDK-cyclin complexes, with CDK1/cyclin B1 (CCNB1) being the one that is essential for mitotic entry and progression. CDK5 is not considered a typical CDK due to its high expression in post-mitotic neurons and activation by non-cyclin proteins p35 and p39. We previously showed that CDK5 is active in mitosis and here we demonstrate that CCNB1 is the mitotic activator of CDK5. Using independent chemical genetic approaches to specifically abrogate CDK5 at the onset of and throughout mitosis, we observe mitotic defects, nuclear atypia, and significant alterations in the mitotic phospho-proteome. Importantly, the disruption of the CDK5-CCNB1 complex phenocopies CDK5 abrogation. Together, our results demonstrate that CCNB1 partners with both CDK5 and CDK1 to drive mitosis, defines CDK5-CCNB1 as a canonical cell cycle CDK/cyclin complex and describes the role of CDK5-CCNB1 complex in ensuring mitotic fidelity.

2025-08-04 | PXD038386 | Pride

Cyclin dependent kinase 5 (CDK5) regulates the circadian clock

Project description:We show that the cyclin-dependent kinase 5 (CDK5) regulates the mammalian circadian clock via phosphorylation of PER2. CDK5 phosphorylated PER2 at serine residue 394 (S394) as shown by an in vitro kinase assay.

2019-12-04 | PXD012068 | Pride

Transcriptional targets of Hippo signaling in mammalian cells

Project description:The Hippo pathway is an emerging signaling cascade involved in the regulation of organ size control. It consists of evolutionally conserved protein kinases that are sequentially phosphorylated and activated. The active Hippo pathway subsequently phosphorylates a transcription coactivator, YAP, which precludes its nuclear localization and transcriptional activation. Identification of transcriptional targets of YAP in diverse cellular contexts is therefore critical to the understanding of the molecular mechanisms in which the Hippo pathway restricts tissue growth. We used microarrays to profile the gene expression patterns upon acute siRNA knockdown of Hippo pathway components in multiple mammalian cell lines and identified a set of genes representing immediate transcriptional targets of the Hippo/Yap signaling pathway. Three mammalian cell lines (HEK293T, HepG2, HaCaT) were transfected with scramble siRNA controls or siRNAs against NF2 and LATS2, two core components of the Hippo pathway, simultaneously. Total RNAs were harvested four days after transfection to reveal the gene expression pattern unsing microarry. YAP and TAZ siRNAs were also transfected along with NF2 and LATS2 siRNAs to identify YAP/TAZ-dependent transcriptional targets upon loss of NF2/LATS2.

2013-12-31 | E-GEOD-49384 | biostudies-arrayexpress

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