Induction and Differentiation of an Epithelial Tumour in the Newt (<i>Triturus cristatus</i>)

Seilern-Aspang, F.; Kratochwil, Klaus

doi:10.1242/dev.10.3.337

Cited by 19 publications

(9 citation statements)

References 18 publications

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“…15 Seilern-Aspand described the induction of the differentiation of an epithelial tumor in newts and the regression of invasive tumors and metastasis. 16 Noda and colleagues have induced the reversion of ras-transformed cells and characterized genes such as K-rev and RECK which are involved in this process. This approach has led to the identification of potential drugs against cancer.…”

Section: Introductionmentioning

confidence: 99%

Quantitative Proteomic Analysis of Tumor Reversion in Multiple Myeloma Cells

Zhang

Tao

et al. 2010

J. Proteome Res.

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Tumor reversion is defined as the process by which cancer cells lose their malignant phenotype. However, relatively little is known about the cellular proteome changes that occur during the reversion process. A biological model of multiple myeloma (MM) reversion was established by using the H-1 parvovirus as a tool to select for revertant cells from MM cells. Isolated revertant cells displayed a strongly suppressed malignant phenotype both in vitro and in vivo. To explore possible mechanisms of MM reversion, the protein profiles of the revertant and parental MM cells were compared using a quantitative proteomic strategy termed SILAC-MS. Our results revealed that 379 proteins were either activated or inhibited during the reversion process, with a much greater proportion of the proteins, including STAT3, TCTP, CDC2, BAG2, and PCNA, being inhibited. Of these, STAT3, which is significantly down regulated, was selected for further functional studies. Inhibition of STAT3 expression by RNA interference resulted in suppression of the malignant phenotype and concomitant down regulation of TCTP expression, suggesting that myeloma reversion operates, at least in part, through inhibition of STAT3. Our results provide novel insights into the mechanisms of tumor reversion and suggest new alternative approaches for MM treatment.

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Section: Introductionmentioning

confidence: 99%

Quantitative Proteomic Analysis of Tumor Reversion in Multiple Myeloma Cells

Zhang

Tao

et al. 2010

J. Proteome Res.

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“…The disadvantage of the discharging mitochondria method is that after discharge, driven by uncontrolled atavistic functionalities, cancerous cell fates are most likely still active; In order to regain control over atavistic functionalities of the unicellular layer, functionalities of the multicellular layer should be reconstructed and reactivated. This idea is related to an old concept of tumor reversion [ 98 ]. Studies demonstrated that when tumor cells are placed within a “normal” morphogenetic milieu, they can be “reprogrammed” (thus acquiring a healthy phenotype de novo) and can then behave as native cells [ 99 ].…”

Section: Discussionmentioning

confidence: 99%

Life Entrapped in a Network of Atavistic Attractors: How to Find a Rescue

Kasperski

2022

IJMS

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In view of unified cell bioenergetics, cell bioenergetic problems related to cell overenergization can cause excessive disturbances in current cell fate and, as a result, lead to a change of cell-fate. At the onset of the problem, cell overenergization of multicellular organisms (especially overenergization of mitochondria) is solved inter alia by activation and then stimulation of the reversible Crabtree effect by cells. Unfortunately, this apparently good solution can also lead to a much bigger problem when, despite the activation of the Crabtree effect, cell overenergization persists for a long time. In such a case, cancer transformation, along with the Warburg effect, may occur to further reduce or stop the charging of mitochondria by high-energy molecules. Understanding the phenomena of cancer transformation and cancer development has become a real challenge for humanity. To date, many models have been developed to understand cancer-related mechanisms. Nowadays, combining all these models into one coherent universal model of cancer transformation and development can be considered a new challenge. In this light, the aim of this article is to present such a potentially universal model supported by a proposed new model of cellular functionality evolution. The methods of fighting cancer resulting from unified cell bioenergetics and the two presented models are also considered.

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“…Moreover, the modulation of the NF-κB signaling and the suppression of the activities of the polycomb protein EZH2 resulted in enhanced differentiation of nasopharyngeal carcinoma cells in vitro via epigenetic mechanisms [231]. Epithelial tumors can regress by differentiation after their implantation in normal tissues [232]. The hypothesis argues that the combined effects of the ECM and epithelial cells over the activity of NF-κB result in its downregulation and the partial recovery of differentiation.…”

Section: Demystifying Tumor Heterogeneity and Resistancementioning

confidence: 99%

Revisiting Epithelial Carcinogenesis

Méndez-López

2022

IJMS

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The origin of cancer remains one of the most important enigmas in modern biology. This paper presents a hypothesis for the origin of carcinomas in which cellular aging and inflammation enable the recovery of cellular plasticity, which may ultimately result in cancer. The hypothesis describes carcinogenesis as the result of the dedifferentiation undergone by epithelial cells in hyperplasia due to replicative senescence towards a mesenchymal cell state with potentially cancerous behavior. In support of this hypothesis, the molecular, cellular, and histopathological evidence was critically reviewed and reinterpreted when necessary to postulate a plausible generic series of mechanisms for the origin and progression of carcinomas. In addition, the implications of this theoretical framework for the current strategies of cancer treatment are discussed considering recent evidence of the molecular events underlying the epigenetic switches involved in the resistance of breast carcinomas. The hypothesis also proposes an epigenetic landscape for their progression and a potential mechanism for restraining the degree of dedifferentiation and malignant behavior. In addition, the manuscript revisits the gradual degeneration of the nonalcoholic fatty liver disease to propose an integrative generalized mechanistic explanation for the involution and carcinogenesis of tissues associated with aging. The presented hypothesis might serve to understand and structure new findings into a more encompassing view of the genesis of degenerative diseases and may inspire novel approaches for their study and therapy.

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Induction and Differentiation of an Epithelial Tumour in the Newt (Triturus cristatus)

Cited by 19 publications

References 18 publications

Quantitative Proteomic Analysis of Tumor Reversion in Multiple Myeloma Cells

Quantitative Proteomic Analysis of Tumor Reversion in Multiple Myeloma Cells

Life Entrapped in a Network of Atavistic Attractors: How to Find a Rescue

Revisiting Epithelial Carcinogenesis

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