The Complex Nature of Breast Cancer Stem-Like Cells: Heterogeneity and Plasticity

French, Rhiannon

doi:10.4172/2157-7633.s7-009

Cited by 9 publications

(5 citation statements)

References 49 publications

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“…For HNSCC, this theory of different CSC phenotypes was first suggested by Biddle et al (32). This hypothesis has also been discussed for breast (33,34) and colorectal (30) cancer. Different phenotypes would make it more difficult to determine the CSC population.…”

Section: Discussionmentioning

confidence: 94%

Expression of ALDH1A1 and CD44 in primary head and neck squamous cell carcinoma and their value for carcinogenesis, tumor progression and cancer stem cell identification

et al. 2015

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Abstract. In head and neck squamous cell carcinoma (HNSCC), aldehyde dehydrogenase 1 family, member A1 (ALDH1A1) and hyaluronan receptor cluster of differentiation 44 (CD44) are often used as cancer stem cell (CSC) markers. The aim of the present study was to examine the relevance of these proteins for HNSCC in general and for the identification of CSCs. Tumors from 48 patients with primary HNSCC were analyzed for the expression of ALDH1A1 and CD44. Additionally, the association of the proteins with the proliferation rate and epidermal growth factor receptor (EGFR) expression was analyzed. ALDH1A1 was expressed in 54.2% of the carcinoma samples while CD44 was expressed in 89.6% of the carcinoma samples. Most notably, these proteins were often not expressed exclusively in a subpopulation, but also in the majority of tumor cells (ALDH1A1: 30.8% of ALDH1A1 + tumors; CD44: 65.1% of CD44 + tumors). Furthermore, patients with ALDH1A1 + tumors exhibited worse survival rates. CD44 and EGFR expression patterns were overlapping within the tumors and the expression rates were significantly connected. Ki-67 + tumor cells often expressed CD44. ALDH1A1 and CD44 expression patterns only partly overlapped. Consequently, ALDH1A1 and CD44 play significant roles in carcinogenesis and tumor progression. Within the present study, CD44 appeared to interact with EGFR and was more often expressed in primary HNSCC than the marker ALDH1A1. However, ALDH1A1 was a better marker to define a subpopulation of tumor cells. Finally, neither ALDH1A1 nor CD44, alone or combined, were sufficient to determine the CSC population in HNSCC.

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Section: Discussionmentioning

confidence: 94%

Expression of ALDH1A1 and CD44 in primary head and neck squamous cell carcinoma and their value for carcinogenesis, tumor progression and cancer stem cell identification

et al. 2015

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“…Although EMT broadly occurs via a progressive directionality as pointed out in previous sections, an interesting interplay is While major incidences of cancer stem cells (CSCs) have been reported to be mesenchymal in nature, one of its many reasons is attributed to the EMT process itself contributing to the generation of CSCs. 13,80 However, notionally, the CSC has multiple origins. 81 Normal stem cells have also been seen to be one of the sources of CSCs.…”

Section: Mathematical Modelmentioning

confidence: 99%

Modeling continuum of epithelial mesenchymal transition plasticity

et al. 2016

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Living systems respond to ambient pathophysiological changes by altering their phenotype, a phenomenon called 'phenotypic plasticity'. This program contains information about adaptive biological dynamism. Epithelial-mesenchymal transition (EMT) is one such process found to be crucial in development, wound healing, and cancer wherein the epithelial cells with restricted migratory potential develop motile functions by acquiring mesenchymal characteristics. In the present study, phase contrast microscopy images of EMT induced HaCaT cells were acquired at 24 h intervals for 96 h. The expression study of relevant pivotal molecules viz. F-actin, vimentin, fibronectin and N-cadherin was carried out to confirm the EMT process. Cells were intuitively categorized into five distinct morphological phenotypes. A population of 500 cells for each temporal point was selected to quantify their frequency of occurrence. The plastic interplay of cell phenotypes from the observations was described as a Markovian process. A model was formulated empirically using simple linear algebra, to depict the possible mechanisms of cellular transformation among the five phenotypes. This work employed qualitative, semi-quantitative and quantitative tools towards illustration and establishment of the EMT continuum. Thus, it provides a newer perspective to understand the embedded plasticity across the EMT spectrum.

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“…Besides, the phenotypic transitions between different NSCCs in breast cancer was reported both in vivo and in vitro [21]. These various types of phenotypic conversions among cancer cells, also known as cancer cell plasticity mechanisms [22], provide new thinking about the CSC hypothesis and related therapeutic strategy [23].…”

Section: Introductionmentioning

confidence: 99%

A multi-phenotypic cancer model with cell plasticity

Zhou

Wang

Wu³

2014

Journal of Theoretical Biology

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The conventional cancer stem cell (CSC) theory indicates a hierarchy of CSCs and non-stem cancer cells (NSCCs), that is, CSCs can differentiate into NSCCs but not vice versa. However, an alternative paradigm of CSC theory with reversible cell plasticity among cancer cells has received much attention very recently. Here we present a generalized multi-phenotypic cancer model by integrating cell plasticity with the conventional hierarchical structure of cancer cells. We prove that under very weak assumption, the nonlinear dynamics of multi-phenotypic proportions in our model has only one stable steady state and no stable limit cycle. This result theoretically explains the phenotypic equilibrium phenomena reported in various cancer cell lines. Furthermore, according to the transient analysis of our model, it is found that cancer cell plasticity plays an essential role in maintaining the phenotypic diversity in cancer especially during the transient dynamics. Two biological examples with experimental data show that the phenotypic conversions from NCSSs to CSCs greatly contribute to the transient growth of CSCs proportion shortly after the drastic reduction of it. In particular, an interesting overshooting phenomenon of CSCs proportion arises in three-phenotypic example. Our work may pave the way for modeling and analyzing the multi-phenotypic cell population dynamics with cell plasticity.

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The Complex Nature of Breast Cancer Stem-Like Cells: Heterogeneity and Plasticity

Cited by 9 publications

References 49 publications

Expression of ALDH1A1 and CD44 in primary head and neck squamous cell carcinoma and their value for carcinogenesis, tumor progression and cancer stem cell identification

Expression of ALDH1A1 and CD44 in primary head and neck squamous cell carcinoma and their value for carcinogenesis, tumor progression and cancer stem cell identification

Modeling continuum of epithelial mesenchymal transition plasticity

A multi-phenotypic cancer model with cell plasticity

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