Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gomisin G inhibits pancreatic cancer cell growth through the Hippo-YAP signaling pathway

ABSTRACT: Purpose: The purpose of this study was to investigate the effect of Gomisin G on the transcription level of pancreatic cancer cells SW1990.

ORGANISM(S): Homo sapiens

PROVIDER: GSE270676 | GEO | 2024/06/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gomisin G inhibits pancreatic cancer cell growth through the Hippo-YAP signaling pathway

Project description:Gomisin G inhibits pancreatic cancer cell growth through the Hippo-YAP signaling pathway

| PRJNA1127671 | ENA

The Hippo pathway effector YAP inhibits HIF2 signaling and ccRCC tumor growth.

Project description: Not available

| S-EPMC9537283 | biostudies-literature

Verteporfin inhibits YAP-induced bladder cancer cell growth and invasion via Hippo signaling pathway.

Project description:The highly conserved Hippo signaling pathway is one of the most important pathways involved in tumorigenesis and progress. Previous studies show that YAP, the transcriptional coactivator of Hippo pathway, is expressed highly in many clinical bladder cancer tissues and plays crucial role on bladder cancer progress. To find the YAP-specific target drug and its molecular mechanism in bladder cancer, we apply Verteporfin (VP), a YAP specific inhibitor to function as anti-bladder cancer drug and discover that VP is able to inhibit bladder cancer cell growth and invasion in a dosage dependent manner. Moreover, we demonstrate that VP may inhibit bladder cancer cell growth and invasion via repressing target genes' expression of the Hippo signaling pathway. In further study, we provide evidence that VP is able to inhibit excessive YAP induced bladder cancer cell growth and invasion. To address the repressive function of VP against YAP in bladder cancer, we check the target genes' expression and find VP can dramatically repress YAP overexpression induced Hippo pathway target genes' expression. Taken together, we discover that VP inhibits YAP-induced bladder cancer cell growth and invasion via repressing the target genes' expression of Hippo signaling pathway.

| S-EPMC5930467 | biostudies-literature

Resolvin D1 inhibits the proliferation of osteoarthritis fibroblast-like synoviocytes through the Hippo-YAP signaling pathway.

Project description:ObjectiveOsteoarthritis (OA) is a disease characterized by cartilage degradation and structural destruction. Resolvin D1 (RvD1), a specialized proresolving mediator (SPM) derived from omega-3 fatty acids, has been preliminarily proven to show anti-inflammatory and antiapoptotic effects in OA. However, the mechanisms of RvD1 in osteoarthritis fibroblast-like synoviocytes (OA-FLSs) need to be clarified.MethodsSynovial and fibroblast-like synoviocytes were obtained from OA patients and healthy individuals. MTT and EdU assays were performed to determine cell cytotoxicity and proliferation. The protein expression levels of cyclin D1, cyclin B1, PCNA, p53, MMP-13, YAP, p-YAP, and LATS1 were detected by western blot analysis. The release levels of IL-1β were detected by ELISA. The cell cycle was assessed by flow cytometry. Immunofluorescence was used to detect the levels of YAP in OA-FLSs.ResultsRvD1 inhibited OA-FLS proliferation and reduced MMP-13 and IL-1β secretion in the concentrations of 20 nM and 200 nM. Furthermore, RvD1 induced G2 cell cycle arrest in OA-FLSs via the Hippo-YAP signaling pathway and promoted YAP phosphorylation. However, RvD1 had no effects on normal FLSs.ConclusionsRvD1 inhibits OA-FLS proliferation by promoting YAP phosphorylation and protects chondrocytes by inhibiting the secretion of MMP-13 and IL-1β, providing an experimental basis for RvD1 treatment of OA.

| S-EPMC8845241 | biostudies-literature

Atheroprotective laminar flow inhibits Hippo pathway effector YAP in endothelial cells.

Project description:Atherosclerosis is a mechanobiology-related disease that preferentially develops in the aortic arch and arterial branches, which are exposed to disturbed/turbulent blood flow but less in thoracic aorta where the flow pattern is steady laminar flow (LF). Increasing evidence supports that steady LF with high shear stress is protective against atherosclerosis. However, the molecular mechanisms of LF-mediated atheroprotection remain incompletely understood. Hippo/YAP (yes-associated protein) pathway senses and effects mechanical cues and has been reported to be a master regulator of cell proliferation, differentiation, and tissue homeostasis. Here, we show that LF inhibits YAP activity in endothelial cells (ECs). We observed that YAP is highly expressed in mouse EC-enriched tissues (lung and aorta) and in human ECs. Furthermore, we found in apolipoprotein E deficient (ApoE(-/-)) mice and human ECs, LF decreased the level of nuclear YAP protein and YAP target gene expression (connective tissue growth factor and cysteine-rich protein 61) through promoting Hippo kinases LATS1/2-dependent YAP (Serine 127) phosphorylation. Functionally, we revealed that YAP depletion in ECs phenocopying LF responses, reduced the expression of cell cycle gene cyclin A1 (CCNA1) and proinflammatory gene CCL2 (MCP-1). Taken together, we demonstrate that atheroprotective LF inhibits endothelial YAP activation, which may contribute to LF-mediated ECs quiescence and anti-inflammation.

| S-EPMC5116386 | biostudies-literature

Next-generation sequencing analysis of transcriptom in gemcitabine resistant pancreatic cancer cells

Project description:Next-generation sequencing was applied to compare the transcriptom of 1) SW1990 human pancreatic cancer cell lines and its gemcitabine-resistant derivative established with long-term exposure in medium containing 100 nM gemcitabine; 2) TRA-1-81+ cells and TRA-1-81- cells isolated from SW1990 human pancreatic cancer cell line.

2017-03-31 | GSE79953 | GEO

Tubuloside B (Tub B) inhibits migration of HCC cells by inhibiting Hippo-YAP pathway

Project description:Purpose: To date, the biological activity of Tub B has not been fully investigated. We set out to analyze how Tub B regulates gene expression in HepG2 cells. Conclusions: Tub B reduced the expression of Hippo pathway downstream target genes in HepG2 cells.

2023-12-01 | GSE220307 | GEO

The differences between CD166+ pancreatic cancer cells and CD166- cells

Project description:Microarray analyses using CD166+ and CD166- pancreatic cancer cell lines from both Panc-1 and SW1990 cells. We carried out microarray analyses using the CD166+ and CD166- separated cells from both Panc-1 and SW1990. The quality of the RNA samples was evaluated using a 2100 Bioanalyzer (Agilent Technologies, Waldbronn, Germany). We used a Human HT-12v4 Expression BeadChip (Illumina, San Diego, CA) for these analyses. The data were analyzed using BeadStudio software version 3.2.3 (Illumina).

2014-02-25 | E-GEOD-55294 | biostudies-arrayexpress

The differences between CD166+ pancreatic cancer cells and CD166- cells

Project description:Microarray analyses using CD166+ and CD166- pancreatic cancer cell lines from both Panc-1 and SW1990 cells.

2014-02-25 | GSE55294 | GEO

The Hippo pathway target, YAP, promotes metastasis through its TEAD-interaction domain.

Project description:The transcriptional coactivator Yes-associated protein (YAP) is a major regulator of organ size and proliferation in vertebrates. As such, YAP can act as an oncogene in several tissue types if its activity is increased aberrantly. Although no activating mutations in the yap1 gene have been identified in human cancer, yap1 is located on the 11q22 amplicon, which is amplified in several human tumors. In addition, mutations or epigenetic silencing of members of the Hippo pathway, which represses YAP function, have been identified in human cancers. Here we demonstrate that, in addition to increasing tumor growth, increased YAP activity is potently prometastatic in breast cancer and melanoma cells. Using a Luminex-based approach to multiplex in vivo assays, we determined that the domain of YAP that interacts with the TEAD/TEF family of transcription factors but not the WW domains or PDZ-binding motif, is essential for YAP-mediated tumor growth and metastasis. We further demonstrate that, through its TEAD-interaction domain, YAP enhances multiple processes known to be important for tumor progression and metastasis, including cellular proliferation, transformation, migration, and invasion. Finally, we found that the metastatic potential of breast cancer and melanoma cells is strongly correlated with increased TEAD transcriptional activity. Together, our results suggest that increased YAP/TEAD activity plays a causal role in cancer progression and metastasis.

| S-EPMC3443162 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data