Exploring MYC relevance to cancer biology from the perspective of cell competition

Paglia, Simona; Sollazzo, Manuela; Giacomo, Simone Di; Strocchi, Silvia; Grifoni, Daniela

doi:10.1016/j.semcancer.2019.05.009

Cited by 19 publications

(16 citation statements)

References 198 publications

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“…So far, the molecular nature of cell competition has been discussed extensively in Drosophila [21][22][23][24][25], and several driving factors have been identified including c-myc and p53 [26][27][28][29]. In fact, we confirmed augmented expression of c-myc in ACT1 cells (S13 Fig), however, it did not seem to make ACTs cells supercompetitor, since the growth of ACT1 is much slower than NTECs (S2 Fig) . Also, differential expression of Scrib does not appear to be involved as there was no difference between NTECs and ACT1 (S13 Fig) . The p53 gene is mutated in ACT1 cells, so that the p53 protein level is significantly stabilized (S13 Fig) . Together with the mutation in the N-ras gene p53 deregulation could confer the 'winner' phenotype [43], but ACT1 growth was indeed suppressed by the cell competition with NTECs, suggesting that driver mutations may play a different role in different cell context.…”

Section: Plos Onesupporting

confidence: 53%

“…Thus, cell competition is now recognized as a critical player in the development of diseases, such as cancer [8,[20][21][22][23][24][25]. In carcinogenesis, Myc-mediated cell competition is the most wellstudied example [26][27][28][29][30]. Since cells showing higher expression of Myc were demonstrated to cause competitive cell elimination in Drosophila [27,28], many types of cancer cells, which overexpress c-Myc protein [31][32][33][34][35], have been though to enable their expansion in tissues with the aid of c-Myc-mediated super-competition [36,37].…”

Section: Introductionmentioning

confidence: 99%

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Cell competition between anaplastic thyroid cancer and normal thyroid follicular cells exerts reciprocal stress response defining tumor suppressive effects of normal epithelial tissue

et al. 2021

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The microenvironment of an early-stage tumor, in which a small number of cancer cells is surrounded by a normal counterpart milieu, plays a crucial role in determining the fate of initiated cells. Here, we examined cell competition between anaplastic thyroid cancer cells and normal thyroid follicular cells using co-culture method. Cancer cells were grown until they formed small clusters, to which normal cells were added to create high-density co-culture condition. We found that co-culture with normal cells significantly suppressed the growth of cancer cell clusters through the activation of Akt-Skp2 pathway. In turn, cancer cells triggered apoptosis in the neighboring normal cells through local activation of ERK1/2. A bi-directional cell competition provides a suppressive mechanism of anaplastic thyroid cancer progression. Since the competitive effect was negated by terminal growth arrest caused by radiation exposure to normal cells, modulation of reciprocal stress response in vivo could be an intrinsic mechanism associated with tumor initiation, propagation, and metastasis.

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Section: Plos Onesupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Cell competition between anaplastic thyroid cancer and normal thyroid follicular cells exerts reciprocal stress response defining tumor suppressive effects of normal epithelial tissue

et al. 2021

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“…One of the most studied regulators of competition is MYC, a family of proteins that is misregulated and contributes to the development of many cancers. In both flies and humans, overexpression of MYC results in the acquisition of a "superfit" phenotype, enabling these cells to outcompete surrounding normal cells by inducing their elimination (Paglia et al 2020). Subsequent studies showed that loss of the tumor suppressors APC and HIPPO can also induce this "superfit" status (Vermeulen et al 2013;Mamada et al 2015), although these effects may reflect the ability of these alterations to drive the downstream activation of MYC.…”

Section: Cell Competitionmentioning

confidence: 99%

Mutant p53 in cell-cell interactions

2021

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p53 is an important tumor suppressor, and the complexities of p53 function in regulating cancer cell behaviour are well established. Many cancers lose or express mutant forms of p53, with evidence that the type of alteration affecting p53 may differentially impact cancer development and progression. It is also clear that in addition to cell-autonomous functions, p53 status also affects the way cancer cells interact with each other. In this review, we briefly examine the impact of different p53 mutations and focus on how heterogeneity of p53 status can affect relationships between cells within a tumor.

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“…It would appear therefore quite reasonable to expect that alterations in these pathways might cause a defective control in the mechanisms of cell competition and, almost inevitably, a parallel increase in the risk of cancer. As an example, the Myc protein is often overexpressed in human cancer[ 43 ] and is also a known driver of cell competition[ 7 ]. Accordingly, cells with up-regulated Myc can express a super-competitor phenotype[ 23 ] and this could contribute, at least theoretically, towards a neoplastic behavior[ 22 ].…”

Section: Cell Competition In the Pathogenesis Of Cancermentioning

confidence: 99%

Cell competition in liver carcinogenesis

Marongiu¹,

Laconi²

2020

WJH

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Cell competition is now a well-established quality control strategy to optimize cell and tissue fitness in multicellular organisms. While pursuing this goal, it is also effective in selecting against altered/defective cells with putative (pre)-neoplastic potential, thereby edging the risk of cancer development. The flip side of the coin is that the molecular machinery driving cell competition can also be co-opted by neoplastic cell populations to expand unchecked, outside the boundaries of tissue homeostatic control. This review will focus on information that begins to emerge regarding the role of cell competition in liver physiology and pathology. Liver repopulation by normal transplanted hepatocytes is an interesting field of investigation in this regard. The biological coordinates of this process share many features suggesting that cell competition is a driving force for the clearance of endogenous damaged hepatocytes by normal donor-derived cells, as previously proposed. Intriguing analogies between liver repopulation and carcinogenesis will be briefly discussed and the potential dual role of cell competition, as a barrier or a spur to neoplastic development, will be considered. Cell competition is in essence a cooperative strategy organized at tissue level. One facet of such cooperative attitude is expressed in the elimination of altered cells which may represent a threat to the organismal community. On the other hand, the society of cells can be disrupted by the emergence of selfish clones, exploiting the molecular bar codes of cell competition, thereby paving their way to uncontrolled growth.

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Exploring MYC relevance to cancer biology from the perspective of cell competition

Cited by 19 publications

References 198 publications

Cell competition between anaplastic thyroid cancer and normal thyroid follicular cells exerts reciprocal stress response defining tumor suppressive effects of normal epithelial tissue

Cell competition between anaplastic thyroid cancer and normal thyroid follicular cells exerts reciprocal stress response defining tumor suppressive effects of normal epithelial tissue

Mutant p53 in cell-cell interactions

Cell competition in liver carcinogenesis

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