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Efficacy of Polo-life kinase 1 inhibitors in preclinical models of small cell lung cancer

ABSTRACT: Efficacy of Polo-life kinase 1 inhibitors in preclinical models of small cell lung cancer

PROVIDER: PRJNA1122852 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29366108_1.fastq.gz	Fastqsanger.gz
	SRR29366108_2.fastq.gz	Fastqsanger.gz
	SRR29366109_1.fastq.gz	Fastqsanger.gz
	SRR29366109_2.fastq.gz	Fastqsanger.gz
	SRR29366110_1.fastq.gz	Fastqsanger.gz

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Efficacy of Polo-life kinase 1 inhibitors in preclinical models of small cell lung cancer

Project description:Small cell lung cancer (SCLC) remains a significant health problem with more than 180,000 newly afflicted patients worldwide per year. Recurrence following initial frontline therapy is associated with resistance to salvage treatment and remains the area of greatest unmet need for SCLC patients. This study systematically examined the efficacy of three different polo like kinase 1 (PLK1) inhibitors in preclinical models of SCLC. The study uncovered robust in vitro activity of PLK1 inhibitors against SCLC cell lines and confirmed the efficacy in patient-derived xenograft models of platinum sensitive and resistant SCLC. A known challenge of targeted therapies in the clinic is the inevitable development of resistance and loss of efficacy. Therefore, understanding the potential mechanisms driving acquired resistance could offer additional strategies to enhance efficacy, delay the development of resistance or reverse the resistance. We generated lab-derived resistant SCLC cells by continuous exposure of parental cells to increasing concentration of onvansertib and performed RNA-seq to identify potential resistance mechanisms.

2025-02-14 | GSE269636 | GEO

Polo-like kinase inhibitors increase AAV production by halting cell cycle progression

Project description:Recombinant Adeno-associated viruses (rAAV) are commonly used in gene therapy for preclinical research and therapeutic applications. Despite its clinical efficacy, the manufacturing of rAAV faces challenges in productivity and quality, leading to limited availability. In this study, we aimed to identify compounds that increase the capacity of cells to produce AAV9 with a high-throughput small-molecule screening strategy. With the Arrayed Targeted Library for AAV Screening platform, we screened a library of 3,300 small molecules and identified several targets, including cell-cycle modulators, G protein-coupled receptor modulators, histone deacetylate inhibitors, Janus kinase inhibitors, and metabolic modulators. Most notably, we identified Polo-like kinase isoform 1 (PLK1) inhibitors as enhancers of AAV production. PLK1 inhibition using HMN-214 increased AAV production, and was largely consistent across HEK293 cell lines, vector payloads and capsid serotypes. Using cell cycle and RNA-sequencing analysis, we show that PLK1 inhibition halts cells in the G2/M phase and blocks their exit from the M to G1 phase. These findings can be used to develop more cost-effective methods to increase AAV yield during production in the manufacturing process.

2025-01-22 | GSE273692 | GEO

Polo-like kinase 1 inhibitors differentiate triple-negative breast cancer towards a luminal cell fate

Project description:Transcriptomic profiling was applied to investigate the effects of polo-like kinase 1 inhibition in triple-negative breast cancer.

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Polo-like kinase inhibitors increase AAV production by halting cell cycle progression

Project description:Polo-like kinase inhibitors increase AAV production by halting cell cycle progression

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Polo-like kinase 1 inhibitors differentiate triple-negative breast cancer towards a luminal cell fate

Project description:Polo-like kinase 1 inhibitors differentiate triple-negative breast cancer towards a luminal cell fate

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Bulk mitotic ATACseq for Polo-like kinase 1 maintains transcription and chromosomal accessibility during mitosis

Project description:We found that Polo-like kinase 1 (Plk1) activity directly on chromatin sustains global transcription and chromosomal accessibility in mitosis. Inhibition of Plk1 leads to significant overall downregulation of accessibility on mitotic chromosomes, especially at promoter and transcription start site (TSS) regions. Therefore, Plk1 activity sustains global chromosomal accessibility in mitosis, facilitating transcription factor binding and ensuring proper transcriptional activity, which maintains mitotic fidelity.

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Inhibition of aberrantly overexpressed Polo-like kinase 4 is a potential effective treatment for DNA damage repair-deficient uterine leiomyosarcoma

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Down-regulation of Polo-like kinase 4 (PLK4) induces G1 arrest via activation of the p38/p53/p21 signalling pathway in bladder

Project description:We demonstrate that Polo-like kinase 4(PLK4) is overexpressed in human bladder cancer (BC) cell lines and tissues, and its overexpression correlates with poor prognosis. PLK4 inhibition suppresses BC cell growth and induces G1 phase arrest via activating p38/p53/p21 pathway in vitro and in vivo. The data suggest that PLK4 might serve as a novel molecular target for BC treatment.

2021-07-29 | GSE180958 | GEO

Two Forkhead transcription factors regulate cardiac progenitor cell divisions by a Polo kinase-dependent pathway

Project description:The development of a complex organ requires the proper differentiation and production of appropriate numbers of each of its constituent cell types, as well as their correct positioning within the organ. During Drosophila cardiogenesis, all three of these processes are controlled by jumeau (jumu) and Checkpoint suppressor homologue (CHES-1-like), two genes encoding forkhead transcription factors that were discovered utilizing an integrated genetic, genomic and computational strategy which identified 70 novel genes expressed in the developing Drosophila heart. Both jumu and CHES-1-like are required during asymmetric cell division for the derivation of two distinct cardiac cell types from their mutual precursor, and in symmetric cell division to produce yet a third type of heart cell. jumu and CHES-1-like control the division of cardiac progenitors by regulating the activity of Polo, a kinase involved in multiple steps of mitosis. This pathway demonstrates how transcription factors integrate diverse developmental processes during organogenesis. GFP-positive cells were profiled from Stage 11-12 Drosophila embryos of the following two genotypes: twi-GAL4 UAS-2EGFP/UAS-jumu and twi-GAL4 UAS-2EGFP

2012-01-30 | E-GEOD-34946 | biostudies-arrayexpress

Targeting the mitotic kinase NEK2 improves the efficacy of CDK4/6 inhibitors

Project description:Targeting the mitotic kinase NEK2 improves the efficacy of CDK4/6 inhibitors

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