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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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Similar Datasets

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

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

The Hippo pathway kinase LATS1 scaffolds Beclin1 in autophagy regulation in hepatocellular carcinoma

Project description:Autophagy perturbation represents an emerging therapeutic strategy in cancer. The mammalian Hippo pathway is an evolutionary conserved tumor suppressive network, where the kinases LATS1/2 phosphorylate and inactivate oncogenic YAP/TAZ. Here, we demonstrated a pro-survival role of LATS1, but not LATS2, in hepatocellular carcinoma cells in response to sorafenib, a standard care of advanced HCC. Transcriptomic analysis revealed a restrictive role of LATS1 in autophagy regulation in HCC cells. Further, we found that the autophagy regulation by LATS1 was independent of its kinase activity. Instead, LATS1 stabilized autophagy core-machinery component Beclin 1 via promoting a non-canonical form of K27-linked ubiquitination, and consequently, inactive Beclin 1 self-dimer, in a E3 ligase NEDD4 dependent manner. Our study highlights a functional diversity between LATS1 and LATS2 and uncovers a scaffolding role of LATS1 in mediating a cross-talk between Hippo signalling and autophagy in HCC and therapy response.

2019-11-13 | GSE117116 | GEO

LATS1/2 Loss Promote Tumor Immune Evasion in Endometrial Cancer through Downregulating MHC-I Expression

Project description:LATS1/2 is frequently mutated and down-regulated in endometrial cancer (EC), but the contribution of LATS1/2 to endometrial tumor progression remains unclear. Here, we discovered an unexpected role of LATS1/2 in regulating MHC class I expression in EC. We demonstrate that the knockout of LATS1/2 in EC cells resulted in significant down-regulation of multiple genes of MHC/HLA Class I family and leaded to insensitivity to tumor immunotherapy. Furthermore, we found that the regulation of LATS1/2 on MHC/HLA expression does not depend on the classical Hippo pathway but on their direct interaction with STAT1 to phosphorylate STAT1 to promote STAT1 accumulating and moving into the nucleus to enhance the transcriptional activation of IRF1/NLRC5 on MHC-I. The kinase-dead mutant LATS1/2 attenuates STAT1 phosphorylation at Ser727. The expressions of LATS1/2, MHC-I, CD8A and p-STAT1（S727）are positive correlation in tissues of EC confirming our findings furtherly. Furthermore, LATS1/2 expression was negatively correlated with tumor stage in EC tissues. These findings reveal novel molecular mechanisms underlying tumor immunogenicity deficiency and elucidate the potential immunotherapy biomarker targeting LATS1/2 in EC.

2024-02-28 | GSE241847 | GEO

Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis [MARS-seq]

Project description:The tumor suppressor LATS1, whose expression is often downregulated in human breast cancer, helps maintain luminal breast cancer cell identity by keeping basal-specific genes in a closed chromatin state, preventing their spurious activation. This is achieved via interaction of LATS1 with the NCOR1 nuclear corepressor and recruitment of HDAC1,driving histone H3K27 deacetylation near NCOR1-repressed “basal” genes. Consequently, decreased expression of LATS1 elevates the expression of such “basal” genes and promotes luminal-to-basal slippage.

2022-10-19 | GSE195715 | GEO

Breast cancer plasticity is restrictedby a LATS1-NCOR1 repressive axis [ATAC-seq]

2022-10-19 | GSE195714 | GEO

Expression profiling in primary embryonic fibroblasts deficient for the N-terminal truncation of Lats1

Project description:Lats1 and Lats2 are the mediators of the Hippo pathway that regulates tissue growth and proliferation. Lats1 and Lats2 kinases share 85% sequence identity in the kinase domain. However, their non-kinase regions at the N-terminus are distinct except for Lats conserved domain 1 (LCD1) and LCD2, suggesting that their N-terminal regions are important for Lats1/2-specific functions. In this study, we generated Lats1 knockout mice disrupting the N-terminal region containing LCD1 (Lats1M-NM-^TN/M-NM-^TN). We show that some Lats1M-NM-^TN/M-NM-^TN mice were born safely and grew normally. However, mouse embryonic fibroblasts (MEFs) from Lats1M-NM-^TN/M-NM-^TN mice displayed drastic defects in mitosis, showing enhanced centrosome overduplication, chromosomal misalignment, multipolar spindle formation, chromosome bridging, and cytokinesis failure. Moreover, they displayed accelerated cell cycle and cell growth bypassing a cell-cell contact inhibition like tumor cells, and exhibited anchorage independent growth. Indeed, Lats1M-NM-^TN/M-NM-^TN MEFs produced tumors in nude mice after subcutaneous injection, although the tumor growth rate was much slower than ordinary cancer cells. Furthermore, Yap, the key transcriptional co-activator in the Hippo pathway, was overexpressed and retained stable in Lats1M-NM-^TN/M-NM-^TN MEFs under high cell density, and expression of Lats2 mRNA were down-regulated. Total RNAs were extracted from MEFs under high or low cell density using miRNeasy extraction kit (Qiagen). A Dye-swapped experiment was performed by hybridizing complimentary RNA (cRNA) labeled with either Cyanine (Cy) -3 or Cy-5 (Perkin-Elmer) onto Whole Mouse Genome Oligo Microarray (G4122F; Agilent Technologies). Co-hybridizations were performed and data from Cy3 or Cy5 channels were analyzed as normalized signal intensities rather than as log ratios corresponding to each array.

2012-12-17 | E-GEOD-37871 | biostudies-arrayexpress

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