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RCC2 Promotes Prostate Cancer Cell Proliferation and Migration Through Hh/GLI1 Signaling Pathway and Cancer Stem-like Cells

ABSTRACT: RCC2 Promotes Prostate Cancer Cell Proliferation and Migration Through Hh/GLI1 Signaling Pathway and Cancer Stem-like Cells

PROVIDER: PRJNA1032552 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26536709_1.fastq.gz	Fastqsanger.gz
	SRR26536709_2.fastq.gz	Fastqsanger.gz
	SRR26536710_1.fastq.gz	Fastqsanger.gz
	SRR26536710_2.fastq.gz	Fastqsanger.gz
	SRR26536711_1.fastq.gz	Fastqsanger.gz

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Gli1+ progenitors mediate bone anabolic function of teriparatide via Hh and Igf signaling

Project description:Teriparatide, a bioactive fragment of human parathyroid hormone (PTH), is the most widely prescribed bone anabolic drug in the world, but its cellular targets remain incompletely defined. The Gli1+ metaphyseal mesenchymal progenitors (MMPs) are a main source for osteoblasts in postnatal growing mice, but their potential response to teriparatide is unknown. Here, by lineage tracing we find that teriparatide stimulates both proliferation and osteoblast differentiation of MMPs. Single-cell RNA sequencing reveals heterogeneity among MMPs including a chondrocyte-like osteoprogenitor (herein COP) population that expands in response to teriparatide. COPs express the highest level of Hedgehog (Hh) target genes and the insulin-like growth factor receptor Igf1r. Inhibition of Hh signaling, or selective deletion of Igf1r in MMPs diminishes the proliferative and osteogenic effects of teriparatide. The study therefore identifies MMPs as teriparatide target cells wherein Hh and Igf signaling are critical for osteoblast production.

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Inhibiting Hh signaling in Gli1+ osteogenic progenitors alleviates TMJOA

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Expression data from regenerating prostates of wild-type or Gli1-/- mutant mice

Project description:Attenuation of Hedgehog (Hh) pathway activity leads to increased prostate branching during adult prostate regeneration. In order to identify genes regulated by the Hh pathway that might be involved in adult prostate branching, we performed transcriptional profiling of regenerating prostates from wild-type or Gli1-/- mutant mice, which have attenuated Hh pathway activity. 6 total samples were analyzed. 3 wild-type prostates and 3 Gli-/- mutant prostates were analyzed.

2014-10-31 | E-GEOD-59849 | biostudies-arrayexpress

Inhibiting Hh signaling in Gli1+ osteogenic progenitors alleviates TMJOA

Project description:The goal of this study is to investigate the role of Gli1+ osteogenic progenitors in the development of TMJOA.

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Expression data from regenerating prostates of wild-type or Gli1-/- mutant mice

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Expression data from the bladders of carcinogen-treated mice with genetic Hh pathway manipulation

Project description:Attenuation of Hedgehog (Hh) pathway activity leads to accelerated tumor progression in a mouse model of N-butyl-N-4-hydroxybutyl nitrosamine (BBN) – induced bladder carcinoma. In order to identify genes regulated by the Hh pathway that might be involved in bladder cancer progression, we performed transcriptional profiling of bladders harvested from mice after BBN-exposure, comparing Gli1CreER/WT; Smoflox/WT mice to Gli1CreER/WT; Smoflox/flox mice, which express CreER under control of the Gli1 promoter and carry one or two floxed alleles of the essential Hh pathway transductory component Smoothened (Smo) respectively. Administration of Tamoxifen to these mice results in attenuation of Hh pathway activty to a greater extent in the Gli1CreER/WT;Smoflox/flox mice as compared to Gli1CreER/WT;Smoflox/WT mice, allowing identification of Hh-pathway regulated genes. 6 total samples were analyzed. 3 bladders from Gli1CreER/WT; Smoflox/WT mice and 3 bladders from Gli1CreER/WT; Smoflox/flox mice were analyzed.

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Project description:T-cell acute lymphoblastic leukemia (T-ALL) is a highly malignant pediatric leukemia, where few therapeutic options are available for patients which relapse. The evolutionarily conserved Hedgehog (Hh) pathway plays a crucial role in patterning and organogenesis during early development, in adult tissue maintenance and repairing functions. Once Hh ligands bind to PTCH1/2 on target cells, the inhibition of Patched proteins for Smo is relieved. Smo translocates to the primary cilium and leads to the breakdown of a protein complex formed by Suppressor of Fused (SUFU) and GLI proteins. GLI transcription factors (GLI1-3) are released and translocate to the nucleus, initiating transcription of Hh target genes. GLI2 and GLI3 have transcriptional activation and repression properties, while GLI1 is a strong positive regulator of Hh transcriptional targets. In T-ALL rare hedgehog pathway mutations have been observed and approximately 20% of T-ALL cases present with ectopic expression of Hh pathway ligands and GLI1. However, the function of Hh signaling and in particular GLI transcription factors in T-ALL initiation and/or tumor progression is not well-known. RNA sequencing was performed in the CUTLL1 T-ALL cell line after knocking out GLI1 gene using CRISPR/Cas9 system.

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Keloid fibroproliferative properties are dependent on stem cells modified by the HEDGEHOG-GLI1 pathway [EA1488]

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