Review old bone, new tricks

Barsky, Livnat; Cohen-Erez, Ifat; Bado, Igor; Zhang, Xiang H.-F.; Vago, Razi

doi:10.1007/s10585-022-10176-5

Cited by 3 publications

(2 citation statements)

References 103 publications

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“…It is somewhat surprising that in the case of MCF7, a less aggressive cell line, on day 7, there is an apparent immunofluorescent signal for all analyzed genes. This could be explained by the capacity of these Luminal A BCCs to acquire a more tumorigenic state, which in our case is reflected by the set of the monitored genes and their invasive potential following the interactions with the BMM . It is also interesting since the Luminal A subtype has a strong bone metastatic organotropism .…”

Section: Discussionsupporting

confidence: 89%

“…This could be explained by the capacity of these Luminal A BCCs to acquire a more tumorigenic state, which in our case is reflected by the set of the monitored genes and their invasive potential following the interactions with the BMM. 33 It is also interesting since the Luminal A subtype has a strong bone metastatic organotropism. 34 In addition, the steep decrease in the proliferation-related genes between days 7 and 14 is also supported by the cell cycle and Fucci reporter analyses.…”

Section: Discussionmentioning

confidence: 99%

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Bone Endosteal Mimics Regulates Breast Cancer Development and Phenotype

Ben Ghedalia Peled,

Hoffman,

Barsky

et al. 2024

Biomacromolecules

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Bone is a frequent site for metastatic development in various cancer types, including breast cancer, with a grim prognosis due to the distinct bone environment. Despite considerable advances, our understanding of the underlying processes leading to bone metastasis progression remains elusive. Here, we applied a bioactive three-dimensional (3D) model capable of mimicking the endosteal bone microenvironment. MDA-MB-231 and MCF7 breast cancer cells were cultured on the scaffolds, and their behaviors and the effects of the biomaterial on the cells were examined over time. We demonstrated that close interactions between the cells and the biomaterial affect their proliferation rates and the expression of c-Myc, cyclin D, and KI67, leading to cell cycle arrest. Moreover, invasion assays revealed increased invasiveness within this microenvironment. Our findings suggest a dual role for endosteal mimicking signals, influencing cell fate and potentially acting as a double-edged sword, shuttling between cell cycle arrest and more active, aggressive states.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%