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Deletion of Lats1/2 in adult kidney epithelia leads to renal cell carcinoma

ABSTRACT: Deletion of Lats1/2 in adult kidney epithelia leads to renal cell carcinoma

PROVIDER: PRJNA692265 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13441338.fastq.gz	Fastqsanger.gz
	SRR13441339.fastq.gz	Fastqsanger.gz
	SRR13441340.fastq.gz	Fastqsanger.gz
	SRR13441341.fastq.gz	Fastqsanger.gz
	SRR13441342.fastq.gz	Fastqsanger.gz

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Deletion of Lats1/2 in adult kidney epithelia leads to renal cell carcinoma

Project description:We characterized the transcriptomes of both primary tumors and lung metastases tha developed in mice following deletion of Lats1 and Lats2 from Slc34a1-expressing cells as well as tumors arising from kidney allografts of and immortalized Lats1-/-;Lats2-/- cell line derived from the renal papilla.

2021-01-15 | GSE164879 | GEO

Deletion of Lats1/2 in adult kidney epithelia leads to renal cell carcinoma.

Project description: Not available

| S-EPMC8159698 | biostudies-literature

miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [PAR-CLIP]

Project description:In this study, we evaluated genetic mouse models of inducible renal epithelia-specific miR-17~92 loss-of-function and gain-of-function using unilateral ureteral obstruction. We utilized PAR-CLIP in HK2 cells to identify miR-17/-20a targets, which we subsequently validated in vitro. We examined expression of a novel miR-17/-20a target in human nephrectomy samples with varying degrees of fibrosis. We identify an activator of Hippo signaling, FERM domain-containing protein 6 (FRMD6, also known as Willin), as a novel miR-17/20a target. Frmd6 is upregulated in tubular epithelium of obstructed kidneys that lack miR-17~92, along with increased phosphorylation of Smad3 and STAT3, two known miR-17~92 profibrotic targets. Frmd6 overexpression is sufficient to result in elevated secretion of the extracellular matrix component collagen III in vitro. Finally, we demonstrate that FRMD6 expression is associated with collagen III expression in human nephrectomy samples.Our findings demonstrate that the miR-17~92 cluster in renal epithelia functions in an anti-fibrotic manner by regulating multiple pro-fibrotic pathways. We also identify Frmd6 as a novel miR-17/20a target in renal epithelia, which may drive renal fibrosis.

2025-01-30 | GSE254785 | GEO

miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [miRNA-seq]

2025-01-30 | GSE254784 | GEO

miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia [RNA-seq]

2025-01-30 | GSE254782 | GEO

Lats1/2 suppress NFkB and aberrant EMT initiation to permit pancreas progenitor differentiation

Project description:The Hippo pathway directs cell differentiation during organogenesis, in part by restricting proliferation. How Hippo signaling maintains a proliferation-differentiation balance in developing tissues and its underlying molecular targets are poorly understood. Our study shows that Hippo suppresses NFκB signaling in pancreatic progenitors to permit cell differentiation and developmental progression. We found that pancreas-specific Lats1/2 kinase deletion (Lats1/2PanKO) from mouse progenitor epithelia results in failure to differentiate 3 key pancreatic lineages: acinar, ductal, and endocrine. We performed an unbiased transcriptome analysis to query the differentiation defects in Lats1/2PanKO. This analysis revealed increased NFκB activator expression, including the pantetheinase Vanin1 (Vnn1). Through in vivo and ex vivo studies, we show that VNN1 activates a detrimental cascade of processes in Lats1/2PanKO epithelium, whereby 1) NFκB activation and 2) initiation of epithelial-to-mesenchymal transition (EMT) together override normal differentiation. We show that exogenous stimulation of VNN1 or NFκB can also trigger this cascade in WT pancreatic progenitors. These findings show that pancreas development requires active suppression of NFκB by LATS1/2 kinases to restrain a cell-autonomous transcriptional program and thereby allow for differentiation.

2019-06-21 | GSE126551 | GEO

Genome-wide analysis of livers of control and Lats1/2 deficient neonatal mice [Microarray expression]

Project description:Lats1-/-;Lats2fl/fl;Alb-Cre pups and control pups were sacrificed at 1 day after birth Total mRNA obtained from livers in control and Lats1/2 deficient neonatal mice

2016-06-29 | E-GEOD-71872 | biostudies-arrayexpress

Genome-wide analysis of gene expression using in vitro cultured control and Lats1/2 deficient hepatoblasts [RNA-Seq]

Project description:RNA-sequencing results with in vitro cultured control and Lats1/2 deficient hepatoblasts, in vitro differentiated control and Lats1/2 deficient hepatocytes and biliary epithelial cells To investigate changes in gene expression by loss of Lats1 and Lats2 during hepatocyte or biliary epithelial cell differentiation, we performed multiplex RNA-sequecing with in vitro cultured hepatoblasts, in vitro differentiated hepatocytes and biliary epithelial cells

2016-06-29 | E-GEOD-71873 | biostudies-arrayexpress

Loss of LATS1 and LATS2 promotes ovarian tumor formation by enhancing AKT activity and PD-L1 expression

Project description:High-grade serous ovarian cancer (HGSOC) is the deadliest and most common subtype of ovarian cancer. Unfortunately, most patients develop recurrence and ultimately resistance to standard platinum chemotherapy. Large tumor suppressors LATS1 and LATS2, the core Hippo signaling kinases, have been implicated in various cancer types, including ovarian cancer. The mechanism by which LATS1/2 suppresses ovarian cancer progression is currently elusive, but the expression of LATS1/2 is frequently reduced or lost in these cancers. In this study, we demonstrate that the inactivation of LATS1/2 is sufficient to transform normal mouse ovarian epithelium into tumorigenic cells associated with increased cell proliferation, invasion and stemness and epithelial–mesenchymal transition (EMT) characteristics. Knockout of Lats1/2 in the epithelial cells also leads to higher expression levels of the immune checkpoint molecule PD-L1, suggesting a regulatory role of LATS1/2 in modulating immune responses and immune evasion. In addition to the loss of LATS1/2 activating the downstream transcriptional coactivators YAP and TAZ, PI3K-AKT activity was also increased, likely contributing to enhanced tumor proliferation and survival. The stimulatory effect of Lats1/2 knockout on cell proliferation can be partially reversed by treatment with the AKT inhibitor MK2206. Treatment with verteporfin, a potent inhibitor of YAP/TAZ, decreases ovarian tumor progression and reduces the activated AKT in the tumors. In summary, this study uncovers several biological mechanisms for the initiation of HGSOC and identifies LATS1/2 as potential prognostic indicators and therapeutic targets.

2025-03-18 | GSE291871 | GEO

miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia

Project description:miR-17/20a mitigates interstitial fibrosis by repressing Frmd6 expression in renal epithelia

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