Aspects of tumor progression

Löser, Thomas

doi:10.1016/j.mehy.2020.110157

Cited by 2 publications

(2 citation statements)

References 43 publications

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“…This justifies the attempt to describe tumor disease and sepsis with a unified disease model. A shift of the paradigm is proposed by choosing the nonspecific innate immune system as the reference point for both diseases Löser (2020). The innate immune system interacts with mutant cells and pathogens.…”

Section: Introductionmentioning

confidence: 99%

Modeling Tumor Disease and Sepsis by Networks of Adaptively Coupled Phase Oscillators

Sawicki

Berner

Löser³

et al. 2022

Front. Netw. Physiol.

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In this study, we provide a dynamical systems perspective to the modelling of pathological states induced by tumors or infection. A unified disease model is established using the innate immune system as the reference point. We propose a two-layer network model for carcinogenesis and sepsis based upon the interaction of parenchymal cells and immune cells via cytokines, and the co-evolutionary dynamics of parenchymal, immune cells, and cytokines. Our aim is to show that the complex cellular cooperation between parenchyma and stroma (immune layer) in the physiological and pathological case can be qualitatively and functionally described by a simple paradigmatic model of phase oscillators. By this, we explain carcinogenesis, tumor progression, and sepsis by destabilization of the healthy homeostatic state (frequency synchronized), and emergence of a pathological state (desynchronized or multifrequency cluster). The coupled dynamics of parenchymal cells (metabolism) and nonspecific immune cells (reaction of innate immune system) are represented by nodes of a duplex layer. The cytokine interaction is modeled by adaptive coupling weights between the nodes representing the immune cells (with fast adaptation time scale) and the parenchymal cells (slow adaptation time scale) and between the pairs of parenchymal and immune cells in the duplex network (fixed bidirectional coupling). Thereby, carcinogenesis, organ dysfunction in sepsis, and recurrence risk can be described in a correct functional context.

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Section: Introductionmentioning

confidence: 99%

Modeling Tumor Disease and Sepsis by Networks of Adaptively Coupled Phase Oscillators

Sawicki

Berner

Löser³

et al. 2022

Front. Netw. Physiol.

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“…Concomitantly, cell growth promoted by PCID2 was also related to inhibition of caspase-dependent apoptosis [ 22 , 23 ]. Besides, PCID2 promotes cell migration/invasion of CRC cells in vitro and formation of lung metastases in nude mice, which is attributed to the induction of epithelial-mesenchymal transition (EMT) by PCID2, thus favoring a mesenchymal phenotype with increased migratory and invasive potential [ 24 – 27 ]. The selective amplification of PCID2 in CRC patients, in conjunction with the compelling oncogenic function of PCID2 in multiple CRC models, collectively indicates a critical role of PCID1 in CRC progression and metastasis.…”

Section: Discussionmentioning

confidence: 99%

A novel amplification gene PCI domain containing 2 (PCID2) promotes colorectal cancer through directly degrading a tumor suppressor promyelocytic leukemia (PML)

Zhang

Zhai

et al. 2021

Oncogene

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Using whole genome sequencing, PCI Domain Containing 2 (PCID2) was identified to be amplified in colorectal cancer (CRC). In this study, we investigated the expression, biological function, molecular mechanism, and clinical implication of PCID2 in CRC. PCID2 mRNA and protein expression were higher in CRC cells and tumor tissues compared to healthy colonic tissues. The copy number of PCID2 was positively correlated with its mRNA expression. Multivariate analysis revealed that PCID2 is an independent prognostic factor for CRC recurrence. Functional studies showed that PCID2 promoted cell growth, cell cycle progression, and cell migration/invasion, while apoptosis was suppressed. Moreover, PCID2 promoted xenograft growth and lung metastasis in nude mice. Using co-immunoprecipitation and mass spectroscopy, we showed that PCID2 binds to promyelocytic leukemia (PML), a tumor suppressor involved in non-canonical β-catenin signaling. PCID2 promoted the degradation of PML via poly-ubiquitination, which in turn, induced Wnt/β-catenin signaling while simultaneously repressing ARF-p53 pathway. Thus, these results demonstrated that PCID2 functions as an oncogene in CRC by enhancing canonical Wnt/β-catenin signaling and inhibition of CTNNB1-ARF-p53 axis. PCID2 promoted canonical Wnt/β-catenin signaling in CRC via degradation of PML. PCID2 may serve as an independent prediction marker for CRC recurrence.

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Aspects of tumor progression

Cited by 2 publications

References 43 publications

Modeling Tumor Disease and Sepsis by Networks of Adaptively Coupled Phase Oscillators

Modeling Tumor Disease and Sepsis by Networks of Adaptively Coupled Phase Oscillators

A novel amplification gene PCI domain containing 2 (PCID2) promotes colorectal cancer through directly degrading a tumor suppressor promyelocytic leukemia (PML)

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