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DNA methylation memory of acinar-ductal transition state altering Kras-downstream Pi3k and Rho GTPase signaling

ABSTRACT: DNA methylation memory of acinar-ductal transition state altering Kras-downstream Pi3k and Rho GTPase signaling

PROVIDER: PRJNA1047540 | ENA |

REPOSITORIES: ENA

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DNA methylation memory of acinar-ductal transition state altering Kras-downstream Pi3k and Rho GTPase signaling [WGBS]

Project description:A critical area of recent cancer research is the emergence of transition states between normal and cancer that exhibit increased cell plasticity which underlies tumor cell heterogeneity. Pancreatic ductal adenocarcinoma (PDAC) arises from a transition state termed acinar-to-ductal metaplasia (ADM), in which digestive enzyme-producing acinar cells acquire a transient ductal epithelium-like phenotype while maintaining their geographical acinar organization. ADM is created by overexpression of the Kruppel-like factor 4 gene (KLF4) in the absence of oncogenic driver mutations. Here, we investigate the DNA methylation landscape and corresponding transcriptional landscape of the mutation-free ADM transition state and the subsequent reversion to a normal acinar phenotype. We ask to what extent cells retain a memory of the ADM transition state via DNA methylation, examine potential regulators of altered DNA methylation during ADM, and investigate the relationship of the ADM transition state to human pancreatic cancer precursor lesions. These findings may inform the mechanisms not only of heritable epigenetic memory of transition states and inflammation, but also of how epigenetic alterations presage or even elicit genetic mutations in cancer.

2025-03-10 | GSE249140 | GEO

DNA methylation memory of acinar-ductal transition state altering Kras-downstream Pi3k and Rho GTPase signaling [spatial transcriptomics]

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DNA methylation memory of acinar-ductal transition state altering Kras-downstream Pi3k and Rho GTPase signaling

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-03-10 | GSE249143 | GEO

Transcriptional regulation by the novel Rho GTPase RhoBTB2.

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TRIM67 drives tumorigenesis in oligodendrogliomas through Rho GTPase-dependent membrane blebbing

Project description:The aim of this study is to characterize the mechanistic role of TRIM67 in glioma biogenesis. Towards this goal, here we utilized engineered human neural stem cells and patient-derived tumor sphere lines with or without IDH mutations and 1p/19q co-deletions to study the function of TRIM67 in gliomas. We found that upregulated TRIM67 induces membrane blebbing through Rho GTPase-mediated signaling, resulting in more advanced cell motility and tumor expansion.

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Quantitative GTPase affinity purification identifies Rho family protein interaction partners

Project description:Although Rho GTPases are essential molecular switches involved in many cellular processes, an unbiased experimental comparison of their interaction partners was not yet performed. Here, we develop quantitative GTPase affinity purification (qGAP) to systematically identify interaction partners of six Rho GTPases (Cdc42, Rac1, RhoA, RhoB, RhoC, RhoD) depending on their nucleotide loading state. We use Stable isotope labeling by Amino acids in cell culture (SILAC) and label free quantification (LFQ). Our interaction network contains many new proteins, reveals highly promiscuous binding of several effectors and mirrors evolutionary relationships of Rho GTPases.

2016-12-23 | PXD004190 | Pride

TRIM67 drives tumorigenesis in oligodendrogliomas through Rho GTPase-dependent membrane blebbing

Project description:TRIM67 drives tumorigenesis in oligodendrogliomas through Rho GTPase-dependent membrane blebbing

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Ota2015 - Positive regulation of Rho GTPase activity by RhoGDIs as a result of their direct interaction with GAPs (GDI integrated)

Project description:This is a ordinary differential equation mathematical model describing the Rho GTPase cycle in which Rho GDP-dissociation inhibitors (RhoGDIs) inhibit the regulatory activities of guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs) by interacting with them directly as well as by sequestering the Rho GTPases. The model was constructed with the intent of analyzing the role of RhoGDIs in Rho GTPase signaling.

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An RNAi Screen for Skin Morphogenesis Unravels The Complexities of Rho GTPase Networks

Project description:During embryogenesis, antagonism and synergy between developmental signaling pathways dictate cell fate decisions. How these circuits orchestrate the complex cellular remodeling needed for tissue morphogenesis remains poorly understood. As effectors of cytoskeletal dynamics, Rho GTPases and their regulators are likely to be involved. However, their daunting complexity has hindered progress in dissecting their functions. Here we overcome this hurdle by developing an unbiased, high throughput RNAi-mediated screening approach to identify physiological regulators of morphogenesis. Exploiting in utero lentiviral delivery methods to transduce embryonic mouse skin progenitors, we screened for Rho GTPases and GTPase regulators that differentially function in epidermal versus hair follicle development. Our screen unveiled hitherto unrecognized roles for specific family members in cytoskeletal remodeling events that impact these diverse morphogenetic processes, including epidermal differentiation, follicle downgrowth and planar cell polarity. Our findings underscore the power of our screening strategy for unravel the physiological significance of complex gene families.

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