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Suppression of CCT3 inhibits tumor growth by downregulating CDK1 expression in melanoma

ABSTRACT: Suppression of CCT3 inhibits tumor growth by downregulating CDK1 expression in melanoma

PROVIDER: PRJNA604922 | ENA |

REPOSITORIES: ENA

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Suppression of CCT3 inhibits tumor growth by downregulating CDK1 expression in melanoma

Project description:The members of the eukaryotic chaperonin family are essential for cell survival. The dysregulation of chaperonin-containing TCP-1 subunit 3 (CCT3) is implicated in the development of several types of malignant tumors. However, its functional role in melanoma remains unknown. Herein, we elucidated the functional contribution of CCT3 to melanoma progression. The results indicated that CCT3 was frequently upregulated in melanoma tissues, and high level of CCT3 is correlated with clinical stage in melanoma patients. Knockdown of CCT3 in melanoma cells markedly inhibited cell proliferation and induced cell apoptosis in vitro and suppressed tumorigenesis in a mouse xenograft model. We also identified the cyclin-dependent kinase 1 (CDK1) as a downstream effector of CCT3 and further evaluation demonstrated that suppression of CCT3 attenuates cell proliferation via downregulating CDK1 expression and CCT3-mediated regulation of cell cycle signaling pathway in melanoma. Collectively, our results provide compelling evidence that CCT3 contributes to melanoma progression via CDK1 and is a potential therapeutic target for melanoma A-375 cells infected with NC lentivirus and CCT3 knockdown lentivirus were prepeared and cultured for RNA extraction and hybridization on Affymetrix microarrays.

2020-02-06 | GSE144788 | GEO

ATF-3 expression inhibits melanoma growth by downregulating ERK and AKT pathways.

Project description: Not available

| S-EPMC8091967 | biostudies-literature

Tight CDK1 inhibition elicits domain-specific pre-RC setting in S-phase, suppressing CFS instability

Project description:Genome integrity requires replication to be completed before chromosome segregation. This coordination essentially relies on replication-dependent activation of a dedicated checkpoint that inhibits CDK1, delaying mitotic onset. Under-replication of Common Fragile Sites (CFSs), however, escapes surveillance, which generates mitotic chromosome breaks. Using human cells, we asked whether this leakage results from insufficient CDK1 inhibition under modest stresses used to destabilize CFSs. We found that tight CDK1 inhibition does suppress CFS instability in so-stressed cells. Molecular combing and Repli-Seq analyses consistently showed a burst of replication initiations in mid S-phase across large origin-poor domains shaped by transcription, including CFSs. CFS rescue and extra-initiations strikingly require availability of essential pre-Replication Complex (pre-RC) proteins during the S-phase, showing that CDK1 inhibition promotes targeted and mistimed pre-RC reloading. In addition to delay mitotic onset, tight checkpoint activation therefore advances replication completion of origin-poor domains at risk of under-replication, two complementary roles preserving genome stability.

2022-12-31 | GSE185282 | GEO

Effect of Cell cycle regulator CDK1 on Cell Differentiation (RNA-IP CDK1 inh KD)

Project description:We addressed the role of cell cycle regulator CDK1 during differentiation by either inhibiting its activity with the specific inhibitor RO3306 (10µM) or by knocking its expression down using specific shRNAs, during mesendoderm differentiation. Human pluripotent stem cells (H9 cells) were synchronized in their cell cycle and then induced to differentiate into mesendoderm for 24h. shRNAs against CDK1 were induced 4 days before starting the differentiation. The CDK1 inhibitor was added to the medium 8h after the induction of differentiation. At the end of the experiment, the cells were harvested and processed for total RNA extraction. RNA-IP was carried out using RiboCluster Profiler RIP-Assay Kit (MBL) following the manufacture’s recommendations.

2021-05-31 | GSE130827 | GEO

Targeted suppression of ZNF217-induced AKT signaling inhibits tumor growth and metastasis in osteosarcoma

Project description:Targeted suppression of ZNF217-induced AKT signaling inhibits tumor growth and metastasis in osteosarcoma

| PRJNA614505 | ENA

Cdk1 controls global epigenetic landscape in embryonic stem cells

Project description:In this study, we found that in ES cells the majority of Cdk1 substrates are localized on chromatin. Cdk1 phosphorylates a large number of proteins involved in epigenetic regulation, including writers and erasers of all major histone marks. High levels of Cdk1 in ES cells phosphorylate and partially inactivate Dot1l, the histone H3 lysine 79 methyltransferase responsible for placing activating H3K79 marks on gene bodies. Decrease of Cdk1 activity during ES cell differentiation de-represses Dot1l, thereby allowing coordinated expression of differentiation genes. These analyses indicate that Cdk1 functions to maintain the epigenetic identity of ES cells.

2020-04-04 | GSE134645 | GEO

Mechanism of nonthermal plasma on melanoma cell growth suppression

Project description:To investigate the miRNAs function in the regulation of nonthermal plasma induced melanoma cell suppression.

2023-07-23 | GSE235507 | GEO

Ailanthone Inhibits Proliferation, Migration and Invasion of Osteosarcoma Cells by Downregulating the Serine Biosynthetic Pathway

Project description:Ailanthone Inhibits Proliferation, Migration and Invasion of Osteosarcoma Cells by Downregulating the Serine Biosynthetic Pathway

| PRJNA786493 | ENA

Small RNA-seq analysis shows reduced tRNA levels in cdk1-as1 mutants

Project description:Purpose: Determine whether Cdk1 only regulates a specific subset of tDNAs, or whether Cdk1 has a more global impact on tDNA expression; Method: We study the expression of tRNA genes in WT cells and cdk1-as1 mutants during S phase by small-RNAseq; Result: We found that expression of at least 77% of all tDNAs is significantly downregulated in S-phase in the cdk1-as1 mutant compared with the WT strain; Conclussions: Cdk1 promotes transcription of the majority of tRNA genes during the cell cycle.

2018-09-10 | GSE116224 | GEO

Regulation of S-phase transcription factors by Cdk1

Project description:Analysis of gene expression across the cell cycle from wild type cells, and cells expressing alleles of Yox1, Yhp1, Hcm1, and Tos4 that cannot be phosphorylated by Cdk1. Expression of S-phase and M/G1 transcripts are downregulated when phosphorylation of these factors is blocked, demonstrating that Cdk1 promotes expression of late cell cycle genes.

2014-04-10 | GSE55121 | GEO

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