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Gene expression data of APC-mutated colorectal cancer patient-derived cells treated with tankyrase inhibitors

ABSTRACT: Tankyrase, a poly(ADP-ribose) polymerase family member, regulates multiple cellular processes. Tankyrase inhibitors efficiently suppress APC-mutated colorectal cancer (CRC) cell proliferation. To examine the mechanism of anti-proliferative effect of tankyrase inhibitors (G007LK and RK582), we analyzed gene expression profiles of patient-derived APC-mutated CRC cells (JC21 and JC475) left untreated or treated with 0.3 µM G007LK or RK582 for 24 h by cDNA microarray analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE232209 | GEO | 2024/01/17

REPOSITORIES: GEO

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Gene expression data of colorectal cancer patient-derived cells treated with tankyrase inhibitors

Project description:Tankyrase, a poly(ADP-ribose) polymerase family member, regulates multiple cellular processes. Tankyrase inhibitors efficiently suppress colorectal cancer (CRC) cell proliferation. To examine the mechanism of anti-proliferative effect of tankyrase inhibitors (G007LK and RK582), we analyzed gene expression profiles of patient-derived CRC cells (JC11 and JC494) left untreated or treated with 0.3 µM G007LK or RK582 for 24 h by cDNA microarray analysis.

2024-01-17 | GSE217758 | GEO

BET protein-dependent E2F pathway confers bell-shaped type resistance to tankyrase inhibitors in APC-mutated colorectal cancer [CUT&RUN]

Project description:In colorectal cancer (CRC), WNT/β-catenin signaling is aberrantly activated mainly by loss-of-function mutations in adenomatous polyposis coli (APC) and is involved in tumor progression. Tankyrase inhibitors, which suppress WNT/β-catenin signaling, are under pre-clinical and clinical trials, while their resistance mechanisms remain unclear. In this study, we established tankyrase inhibitor-resistant CRC cells, JC73-RK100, from APC-mutated patient-derived CRC cells. JC73-RK100 cells and several CRC cells were sensitive to tankyrase inhibitors at low concentrations but were resistant at high concentrations (i.e., bell-shaped dose response: BSDR). Mechanistically, tankyrase inhibitors at high concentrations promoted BRD3/4-dependent E2F target gene transcription and over-activated cell cycle progression in the BSDR cells. BET inhibitors canceled the bell-shaped dose response to tankyrase inhibitors. Taken together, these observations suggest that combination of tankyrase and BET inhibitors would be a useful therapeutic approach to overcome a subset of resistance to tankyrase inhibitors.

2024-07-29 | GSE239680 | GEO

BET protein-dependent E2F pathway confers bell-shaped type resistance to tankyrase inhibitors in APC-mutated colorectal cancer [RNA-seq]

2024-07-29 | GSE239681 | GEO

Expression data of colon cancer COLO320DM cells and tankyrase inhibitor-resistant variant 320-IWR cells

Project description:Wnt/β-catenin signaling is activated in colorectal cancer (CRC) and is involved in CRC growth. Tankyrase, a poly(ADP-ribose) polymerase family member, destabilizes Axin and positively regulates the Wnt/β-catenin signaling. Tankyrase inhibitors efficiently suppress CRC cell proliferation. We established 320-IWR cells, which showed resistance to tankyrase inhibitor IWR-1, from human CRC COLO-320DM cells. We analyzed gene expression profile of 320-IWR cells (320IWR_1,_2) and parental COLO-320DM cells (COLO320_1,_2).

2016-11-01 | GSE86061 | GEO

Tankyrase inhibitors target colorectal cancer stem cells via AXIN-dependent downregulation of c-KIT tyrosine kinase

Project description:Tankyrase, a poly(ADP-ribose) polymerase family member, destabilizes Axin and positively regulates the Wnt/β-catenin signaling. We demonstrated that tankyrase inhibitors can target the colorectal cancer stem-like cells. Tankyrase inhibitors efficiently suppress colorectal cancer stem-like cell proliferation via AXIN-dependent manner. We sorted CD44-positive COLO-320DM cells, which showed a characteristic of CSCs and were targeted by tankyrase inhibitors. We analyzed gene expression profile of CD44-positive cells (CD44-positive 01, 02, 03) and CD44-negative cells (CD44-negative 01, 02, 03).

2020-05-05 | GSE130750 | GEO

Gene expression data of APC-mutated colorectal cancer patient-derived cells treated with tankyrase inhibitors

Project description:Gene expression data of APC-mutated colorectal cancer patient-derived cells treated with tankyrase inhibitors

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Human Tankyrases TAP-LC-MSMS - Proteomic Analysis of the Human Tankyrase Protein Interaction Network Reveals Its Role in Pexophagy

Project description:Tankyrase 1 (TNKS1) and tankyrase 2 (TNKS2) belong to the poly(ADP-ribose) polymerase (PARP) family of proteins, which use NAD+ to modify substrate proteins with ADP-ribose modifications. Tankyrases are implicated involving in multiple cellular functions, including the telomere length control, Wnt/b-catenin pathway regulation, glucose uptake and cell cycle regulation. Emerging evidences reveal the pathological relevance of tankyrase in diseases and propose these two key enzymes as potential drug targets. However, the cellular functions and regulatory machineries of tankyrases are still largely unknown. Through this proteomic analysis, we not only defined the protein-protein interaction map for the tankyrases which revealed 100~150 high confident interacting proteins for tankyrases in various cellular functions, but also uncovered the novel regulating function of tankyrase in peroxisome homeostasis.

2017-07-24 | PXD004647 | Pride

A genome-wide screen for peroxisome regulators connects peroxisomes with Wnt signaling through RNF146 and tankyrase

Project description:Peroxisomes are membrane-bound organelles that help cells specialize their metabolism. In humans, peroxisomes are required for normal development, yet the genes regulating peroxisome function remain unclear. Thus, we performed a genome-wide CRISPRi screen to identify novel factors involved in peroxisomal homeostasis. We found that transcriptional inhibition of RNF146, an E3 ligase activated by poly(ADP-ribose), dramatically reduced the import of proteins into peroxisomes. The observed RNF146-mediated loss of peroxisome import depended on the stabilization and activity of the poly(ADP-ribose) polymerase tankyrase, which binds the peroxisomal membrane protein PEX14. We propose a model in which RNF146 and tankyrase regulate peroxisome import efficiency by tuning PARsylation of proteins at the peroxisome membrane. Interestingly, we found that perturbations to peroxisomes altered tankyrase’s selection of substrates, including the beta-catenin destruction complex component AXIN1. The loss of peroxisomes caused tankyrase and RNF146-dependent degradation of AXIN1 and a concomitant increase of beta-catenin transcription. Together, these observations not only suggest previously undescribed roles for RNF146 in peroxisomal regulation, but also a novel role in bridging peroxisome function with Wnt/beta-catenin signaling during development.

2024-06-01 | GSE266892 | GEO

A genome-wide screen for peroxisome regulators connects peroxisomes with Wnt signaling through RNF146 and tankyrase [Amplicon-sequencing]

2024-06-01 | GSE266855 | GEO

Gene expression profiling of tankyrase-inhibited mouse articular chondrocytes

Project description:Osteoarthritis (OA) is a prevalent degenerative disease, which involves progressive and irreversible destruction of cartilage matrix. Despite efforts to reconstruct cartilage matrix in osteoarthritic joints, it has been a difficult task as adult cartilage exhibits marginal repair capacity. Here we report the identification of tankyrase as a regulator of the cartilage anabolism axis based on systems-level factor analysis of mouse reference populations. Tankyrase inhibition drives the expression of a cartilage-signature matrisome and elicits a transcriptomic pattern that is inversely correlated with OA progression. Furthermore, tankyrase inhibitors ameliorate surgically-induced OA in mice, and stem cell transplantation coupled with tankyrase knockdown results in superior regeneration of cartilage lesions. Mechanistically, the pro-regenerative features of tankyrase inhibition are mainly triggered by uncoupling SOX9 from a poly(ADP-ribosyl)ation (PARylation)-dependent protein degradation pathway. Our findings provide insights into the development of future OA therapies aimed at reconstruction of articular cartilage.

2019-09-24 | GSE137899 | GEO

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