Dynamic equilibrium between cancer stem cells and non-stem cancer cells in human SW620 and MCF-7 cancer cell populations

Yang, Gen; Quan, Yi; Wang, W; Fu, Qibin; Wu, Juanxia; Mei, Tao; Li, J; Tang, Yuxing; Luo, Chunxiong; Ouyang, Qi; Chen, S; Wu, Lijun; Hei, Tom K.; Wang, Y

doi:10.1038/bjc.2012.126

Cited by 96 publications

(132 citation statements)

References 35 publications

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“…The phenotypic plasticity of CSCs is dynamically regulated by intrinsic and extrinsic signals originating from the cancer microenvironment. TGF-␤, a major inducer of EMT, has an important role in the inter-conversion and equilibrium of CSCs and non-CSCs by regulating the EMT process (33). Indeed, we found that TGF-␤ was up-regulated in HA-overproducing cancer cells and that the inhibition of its signaling pathway significantly reduced EMT and CSC conversion.…”

Section: Coordinated Roles Of Snail and Twist In Has2-induced Csc Expmentioning

confidence: 68%

Excessive Hyaluronan Production Promotes Acquisition of Cancer Stem Cell Signatures through the Coordinated Regulation of Twist and the Transforming Growth Factor β (TGF-β)-Snail Signaling Axis

Chanmee

Ontong

Mochizuki

et al. 2014

Journal of Biological Chemistry

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Background: Hyaluronan overproduction is implicated in breast cancer progression. Results: Hyaluronan overproduction expands cancer stem-like cells through the up-regulation of Snail and Twist expression. Conclusion: Hyaluronan overproduction allows plastic cancer cells to revert to stem cell states via Twist and the transforming growth factor ␤-Snail signaling axis. Significance: These findings will help to understand the unique hyaluronan-dependent mechanisms that govern cancer cell plasticity and cancer stem cell expansion.

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Section: Coordinated Roles Of Snail and Twist In Has2-induced Csc Expmentioning

confidence: 68%

Excessive Hyaluronan Production Promotes Acquisition of Cancer Stem Cell Signatures through the Coordinated Regulation of Twist and the Transforming Growth Factor β (TGF-β)-Snail Signaling Axis

Chanmee

Ontong

Mochizuki

et al. 2014

Journal of Biological Chemistry

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“…The initial 200 nm aggregates formed by the relatively rapid nucleation of Zn−hexamer subsequently grow through the further addition of Zn− hexamer to these aggregates, that is, via "nucleation and growth". 55,56 Increase of the temperature to 37°C does not appear to change the mechanism of aggregation but results in a modest increase in the apparent diameter and final turbidity (data not shown). This is consistent with other observations of Zn−insulin aggregating at pH 4−9, although aggregate size did not exceed 20 nm diameter (at I = 100 mM).…”

Section: 53mentioning

confidence: 91%

Effect of Heparin on Protein Aggregation: Inhibition versus Promotion

Seeman

Yan

et al. 2012

Biomacromolecules

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The effect of heparin on both native and denatured protein aggregation was investigated by turbidimetry and dynamic light scattering (DLS). Turbidimetric data show that heparin is capable of inhibiting and reversing the native aggregation of bovine serum albumin (BSA), β-lactoglobulin (BLG), and Zn−insulin at a pH near pI and at low ionic strength I; however, the results vary with regard to the range of pH, I, and protein−heparin stoichiometry required to achieve these effects. The kinetics of this process were studied to determine the mechanism by which interaction with heparin could result in inhibition or reversal of native protein aggregates. For each protein, the binding of heparin to distinctive intermediate aggregates formed at different times in the aggregation process dictates the outcome of complexation. This differential binding was explained by changes in the affinity of a given protein for heparin, partly due to the effects of protein charge anisotropy as visualized by electrostatic modeling. The heparin effect can be further extended to include inhibition of denaturing protein aggregation, as seen from the kinetics of BLG aggregation under conditions of thermally induced unfolding with and without heparin.

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“…Similar observations linking plasticity and EMT have been made in cell lines [36]. More recently, Yang et al [37] have visualised plasticity between non-stem cancer cells and bCSCs occurring in situ in MCF-7 cells and shown that this process could be enhanced by the induction of EMT or perturbed by its inhibition [37].…”

Section: Plasticity Of Breast Cancer Stem-like Cells Plasticity Betwementioning

confidence: 55%

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

French¹

2013

J Stem Cell Res Ther

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There are multiple definitions of cancer stem cells based on the different assays used to detect or enrich for them. The existence of different assays has made the identification and isolation of the archetypal cancer stem cell (CSC) with all of these properties an attractive but as yet unachievable goal. Indeed, it has been suggested that the lack of complementarity between these assays is in itself a barrier to CSC identification. Yet new insights into the heterogeneity of breast cancer stem cells and the discovery of CSC plasticity now suggests that rather than the existence of a single elusive stem-like entity in cancers, there may be a heterogeneous mix of cell populations able to switch their phenotype under different selective pressures. The aim of this review is to summarise the current evidence supporting this hypothesis and to suggest that focusing on the mechanisms controlling the inter-conversion between these minority stem cell populations could lead to more effective strategies to target the malignant properties of breast cancer stem cells.

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Dynamic equilibrium between cancer stem cells and non-stem cancer cells in human SW620 and MCF-7 cancer cell populations

Cited by 96 publications

References 35 publications

Excessive Hyaluronan Production Promotes Acquisition of Cancer Stem Cell Signatures through the Coordinated Regulation of Twist and the Transforming Growth Factor β (TGF-β)-Snail Signaling Axis

Excessive Hyaluronan Production Promotes Acquisition of Cancer Stem Cell Signatures through the Coordinated Regulation of Twist and the Transforming Growth Factor β (TGF-β)-Snail Signaling Axis

Effect of Heparin on Protein Aggregation: Inhibition versus Promotion

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

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