The cancer stem cell phenotype as a determinant factor of the heterotypic nature of breast tumors

Fonseca, Nuno A.; Cruz, Ana F.; Moura, Vera; Simões, Sérgio; Moreira, João Nuno

doi:10.1016/j.critrevonc.2017.03.016

Cited by 33 publications

(21 citation statements)

References 126 publications

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“…As described in a breast cancer study, two distinct populations (epithelial-to-mesenchymal and mesenchymal-toepithelial) of CSCs were found [44]. Current data indicate that CSCs are not fixed at full epithelial or full mesenchymal cell status, but maintain plasticity between EMT and MET states [42,45]. Consequently, tumors are supposed to consist of continuous sequence of cell states along epithelial to mesenchymal positions [46].…”

Section: Cancer Stem Cellsmentioning

confidence: 66%

“…Even more, increasing data show that cells with self-renewal potential can be generated from terminally differentiated somatic cells, thus reverting hierarchical developmental organization. For example, there is evidence that breast CSCs have originated from non-stem cancer cells [42]. Under the regulation of multiple factors, differentiated cancer cells could regain "stemness," in this way confirming bidirectional conversion between non-stem and stem cells [34].…”

Section: Cancer Stem Cellsmentioning

confidence: 99%

“…Deregulated canonical and developmental signaling pathways are highly associated with CSC phenotype and regulation of CSC behavior. Alterations in proliferation, differentiation, and programmed cell death pathways have been demonstrated [42].…”

Section: Cancer Stem Cellsmentioning

confidence: 99%

See 2 more Smart Citations

Recent Approaches Encompassing the Phenotypic Cell Heterogeneity for Anticancer Drug Efficacy Evaluation

Stulpinas¹,

Imbrasaitė²,

Krestnikova³

et al. 2020

Tumor Progression and Metastasis

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Despite the advancements in biomarker-based personalized cancer therapy, the inadequacy of molecular and genetic profiling in identifying effective drug combinations was defined in most cases. Drug resistance remains a major limitation of the current predictive oncology. Emerging reports indicate that the success of anticancer therapy is usually limited by intratumoral heterogeneity which is not captured by the existing cancer cell biomarker-based approaches. Cell heterogeneity, not only genetic but also phenotypic, is considered to be the root cause of resistance to anticancer treatment, cancer progression, and the presence of cancer stem cells. Therefore, functional testing of live cells representing various cell types within the tumor exposed to potential therapies is needed for identification of effective drug combinations. Here we look at the different existing model systems, including ex vivo models of the patient's tumor cells, 2D/3D in vitro cultures/cocultures, patient-derived cellular organoids, single-cell models, ex vivo tumor platforms containing tumor microenvironment and extracellular matrix, etc., scoping at drug efficacy evaluation and solving the problem of cancer resistance.

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Section: Cancer Stem Cellsmentioning

confidence: 66%

Section: Cancer Stem Cellsmentioning

confidence: 99%

See 1 more Smart Citation

Recent Approaches Encompassing the Phenotypic Cell Heterogeneity for Anticancer Drug Efficacy Evaluation

Stulpinas¹,

Imbrasaitė²,

Krestnikova³

et al. 2020

Tumor Progression and Metastasis

View full text Add to dashboard Cite

show abstract

“…Cells in the TME, such as endothelial cells, fibroblasts or even mesenchymal stem cells, are thought to regulate breast CSCs, when they secrete different signaling molecules associated with survival, proliferation or differentiation (30). The constant appearance of CSCs in breast cancer has been associated with signaling pathways associated with embryonic development, such as the Notch and hedgehog pathways.…”

Section: Breast Cancer Stem Cellsmentioning

confidence: 99%

Role of autophagy in breast cancer and breast cancer stem cells (Review)

et al. 2018

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Autophagy is a key catabolic process, in which cytosolic cargo is engulfed by the formation of a double membrane and then degraded through the fusing of autophagosomes with lysosomes. Autophagy is a constitutively active, evolutionarily conserved, catabolic process important for the maintenance of homeostasis in cellular stress responses and cell survival. Although the mechanisms of autophagy have not yet been fully elucidated, emerging evidence suggests that it plays a dual role in breast cancer and in maintaining the activity of breast cancer stem cells (CSCs). However, it may play a complex role in breast CSC therapy. Breast CSCs, a population of cells with the ability to self-renew, differentiate, and initiate and sustain tumor growth, play an essential role in cancer recurrence, anticancer resistance and metastasis. In addition, the elucidation of the association between autophagy and apoptosis in the tumor context is crucial in order to better address appropriate therapy strategies. In the present review, a summary of the mechanisms and roles of autophagy in breast cancer and CSCs is presented. The potential value of such autophagy modulators in the development of novel breast cancer therapies is discussed.

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“…Nucleolin is a multifunctional protein that has a number of important functions in the vital activities of the cell. For example, its involvement in chromatin remodeling, mRNA stabilization and translational modulation has been shown [Fonseca et al 2015;Fonseca et al 2017]. Nucleolin studies have shown that its N-terminal domain regulates transcription and maturation of ribosomal RNA [Roger et al 2003].…”

Section: Introductionmentioning

confidence: 99%

Different localization of fluorescently labeled N- and C-termini of nucleolin variants in human glioblastoma cell culture

Panteleev

Pustogarov

Revishchin

et al. 2019

Preprint

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Nucleolus-oriented protein nucleolin plays a significant role in the life of a normal mammalian cell. However, nucleolin is also actively expressed in cells of malignant tumors. At the same time, its expression in different types of cancer is significantly increased compared with normal cells. It is interesting that nucleolin localization often varies in tumor cells, namely in the cytoplasm and on the cell membrane. This fact is considered to be a poor prognostic indicator. This work is devoted to the study of the distribution of nucleolin in human glioblastoma cells. Glioblastoma is one of the most aggressive malignant tumors with an absolutely unfavorable prognosis. These tumors have a high proliferative potential, but in addition they are often characterized by invasive properties. Research on lineage cells does not let to fully study these properties of glioblastoma, since lineage cells are very different from the actual tumor. In our study, we used two primary cell cultures of human glioblastoma with varying degrees of invasiveness of the original tumors. The main interest was directed at studying the localization of nucleolin and its correlation with the invariability of the N- and C-termini of the corresponding protein. Particular attention was paid to the significance of the unaltered C-terminus of nucleolin for its distribution in the cells of transplanted human glioblastoma cultures derived from patient tissues.The aim of this work is to find the relationship between the deformation of the N- or C-terminal sequences of nucleolin and its localization.We showed that in glioblastoma cells, with a high degree of invasion, nucleolin is found in the cytoplasm and close to the cell membrane, and the distribution of nucleolin with undeformed C and N-terminal does not match.

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The cancer stem cell phenotype as a determinant factor of the heterotypic nature of breast tumors

Cited by 33 publications

References 126 publications

Recent Approaches Encompassing the Phenotypic Cell Heterogeneity for Anticancer Drug Efficacy Evaluation

Recent Approaches Encompassing the Phenotypic Cell Heterogeneity for Anticancer Drug Efficacy Evaluation

Role of autophagy in breast cancer and breast cancer stem cells (Review)

Different localization of fluorescently labeled N- and C-termini of nucleolin variants in human glioblastoma cell culture

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