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Effect of PI3K/mTOR dual-target inhibitor WX390 on adipose-derived stem cells isolated from facial infiltrating lipomatosis

ABSTRACT: Effect of PI3K/mTOR dual-target inhibitor WX390 on adipose-derived stem cells isolated from facial infiltrating lipomatosis

PROVIDER: PRJNA1064148 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27532284_1.fastq.gz	Fastqsanger.gz
	SRR27532284_2.fastq.gz	Fastqsanger.gz
	SRR27532285_1.fastq.gz	Fastqsanger.gz
	SRR27532285_2.fastq.gz	Fastqsanger.gz
	SRR27532286_1.fastq.gz	Fastqsanger.gz

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Effect of PI3K/mTOR dual-target inhibitor WX390 on adipose-derived stem cells isolated from facial infiltrating lipomatosis

Project description:Facial infiltrating lipomatosis (FIL) is a congenital disorder characterized by unilateral facial enlargement. Although next-generation sequencing has revealed that the pathogenesis of FIL is associated with phosphatidylinositol 3-kinase catalytic subunit alpha (PIK3CA) mutations, the underlying molecular mechanisms remain undetermined. We found that the adipose tissue in FIL patients demonstrated tissue infiltration accompanied by adipocytes hypertrophy and increased lipid accumulation. All FIL-ADSCs harboured PIK3CA mutations. Compared to ADSCs obtained from normal subcutaneous adipose tissue, FIL-ADSCs exhibited a greater capacity for adipogenesis. Suppression of PIK3CA resulted in a reduction in the adipogenic potential of FIL-ADSCs. Furthermore, WX390, a novel dual-target PI3K/mTOR inhibitor, was found to impede PIK3CA-mediated adipogenesis both in vivo and in vitro. RNA-seq revealed that the expression of transient receptor potential vanilloid subtype 1 (TRPV1) was upregulated after PI3K pathway inhibition, and overexpression and activation of TRPV1 both inhibited adipogenesis of FIL-ADSCs. Our study showed that PIK3CA mutations promoted adipogenesis in FIL-ADSCs and that this effect was achieved by suppressing the expression of TPRV1. Pathogenesis experiments suggested that WX390 may serve as an agent for the treatment of FIL.

2024-06-28 | GSE253170 | GEO

Comparative study of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in MCL

Project description:Phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway activation contributes to mantle cell lymphoma (MCL) pathogenesis and drug resistance. However, the use of mTOR inhibitors as single agents have shown limited clinical efficacy in relation with drug activation of feedback loops. Selective PI3K inhibition or dual PI3K/mTOR catalytic inhibition are different therapeutic approaches developed to achieve effective pathway blockage. Here, we evaluated the antitumor activity of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in primary MCL cells. We found that dual PI3K/mTOR inhibitor modulated angiogenesis, tumor invasiveness and cytokine signaling compared to a mTOR inhibitor and a pan-PI3K inhibitor in MCL. We used microarrays to compare the effect of these three compounds in MCL and identified distinct classes of down-regulated genes modulated by each compound. Global RNA expression in primary cells from two MCL patients treated with a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor for 8 hours

2013-12-14 | E-GEOD-53309 | biostudies-arrayexpress

Comparative study of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in MCL

2013-12-14 | GSE53309 | GEO

Effect of a dual specificity PI3K/mTOR inhibitor, NVP-BEZ235, on human ovarian cancer cell lines grown in 3D culture

Project description:Analysis of the effects of a dual specificity PI3K/mTOR inhibitor on two human ovarian cell lines, OV2008 and MCAS. Results provide insight into the adaptive response to PI3K/mTOR inhibition in matrix attached ovarian cancer cells. The PI3K/mTOR-pathway is the most commonly deregulated pathway in epithelial cancers and thus represents an important target for cancer therapeutics. Here we show that dual inhibition of PI3K/mTOR in ovarian cancer 3D-spheroids leads to death of the inner matrix-deprived cells, whereas matrix-attached cells are resistant. Resistance is associated with up-regulation of a cellular survival program that involves both FOXO-regulated transcription and a novel translational resistance mechanism resulting in specific up-regulation of IRES-mediated, cap-independent translation. Inhibition of any of several up-regulated proteins, including Bcl-2, EGFR, or IGF1R, abrogates resistance to dual PI3K/mTOR inhibition. These results demonstrate that acute adaptive response to PI3K/mTOR inhibition resembles well-conserved adaptive response to nutrient and growth factor deprivation and how development of rational drug combinations can bypass resistance mechanisms. Total RNA was isolated 6h and 24h after treatment with 1 M-NM-<M NVP-BEZ235 or DMSO vehicle control from 3D grown structures

2012-03-13 | E-GEOD-28992 | biostudies-arrayexpress

Effect of a dual specificity PI3K/mTOR inhibitor, NVP-BEZ235, on human ovarian cancer cell lines grown in 3D culture

2012-03-13 | GSE28992 | GEO

Response to PI3K/mTOR dual inhibition in Glioma initiating cells

Project description:The PI3K/mammalian target of rapamycin (mTOR) pathway is dysregulated in over 50% of human GBM but remains a challenging clinical target. Inhibitors against PI3K/mTOR mediators have limited clinical efficacy as single agents. Gene expression profiling after PI3K/mTOR inhibition treatment was analyzed by Affymetrix microarrays.

2016-05-20 | GSE79316 | GEO

PQR309 is a novel dual PI3K/mTOR inhibitor with antitumor pre-clinical activity in lymphomas as single agent and in combination

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Resistance to PI3K/mTOR inhibitor PF-04691502 in KRAS mutant colorectal cancer models reveals a sensitivity to combination with EGFR inhibition

Project description:We explored potential bypass mechanisms to PI3K/mTOR-directed therapy in KRAS mutant CRC models, utilizing genetically engineered mouse models (GEMM) to generate acquired resistance to the targeted dual PI3K/mTOR small molecule inhibitor PF-04691502. Transcriptomic analysis revealed a dynamic stem-like progenitor signature which was increased in the presence of drug pressure.

2014-08-31 | E-MTAB-2510 | biostudies-arrayexpress

SUM52PE treated with PI3K-mTOR inhibitors

Project description:SUM52PE treated with PI3K-mTOR inhibitors

| PRJNA509669 | ENA

Omipalisib Inhibits Esophageal Cancer Growth through PI3K/AKT/mTOR Signalling Pathway Disruption

Project description:Esophageal squamous cell carcinoma (OSCC) is a lethal digestive tract malignancy with limited effective interventions. This study aims to explore a new potential inhibitor on OSCC and investigate the underlying mechanisms. Based on a drug screen of an FDA-proven library consisting of 1404 compounds, we demonstrated that Omipalisib, a dual PI3K/mTOR inhibitor, markedly inhibited cell proliferation and colony formation in a panel of OSCC cell lines. Mechanistically, Omipalisib induced G0/G1 phase cell cycle arrest and apoptosis. Moreover, RNA-seq, KEGG and GSEA confirmed that the PI3K/mTOR signalling pathway is the primary target of Omipalisib in OSCC cells. Omipalisib treatment suppressed the PI3K/mTOR signalling pathway. Furthermore, Omipalisib exerted a significant antineoplastic effect on OSCC tumour xenografts in BALB/c nude mice without obvious side effects. The present study supports the rationale for using Omipalisib as a therapeutic approach for OSCC cases and suggests the potential clinical evaluation of this strategy.

2020-01-11 | GSE143462 | GEO

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