Adipose Stem Cells and Cancer: Concise Review

Sabol, Rachel A.; Giacomelli, Paulina; Beighley, Adam; Bunnell, Bruce A.

doi:10.1002/stem.3050

Cited by 25 publications

(24 citation statements)

References 75 publications

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“…We have reported that the differentiation of adipose progenitors (APs), which are a type of mesenchymal stem cells, into myofibroblasts is dependent upon the primary cilium [ 12 ]. APs can also differentiate into CAFs and are found in several organs prone to cancer [ 13 , 14 ]. APs are particularly relevant in breast cancer since the adipose tissue is abundant in this organ and has been shown to be in direct contact with tumors.…”

Section: Introductionmentioning

confidence: 99%

The Primary Cilium of Adipose Progenitors Is Necessary for Their Differentiation into Cancer-Associated Fibroblasts that Promote Migration of Breast Cancer Cells In Vitro

Peraldi

Ladoux

Giorgetti‐Peraldi

et al. 2020

Cells

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Cancer associated fibroblasts (CAFs) are central elements of the microenvironment that control tumor development. In breast cancer, CAFs can originate from adipose progenitors (APs). We, and others, have shown that the primary cilium, an antenna-shaped organelle, controls several aspects of APs’ biology. We studied the conversion of human APs into CAFs by breast cancer cell lines (BCCs). Deletion of the cilium of APs by a pharmacological inhibitor, or by siRNA, allow us to demonstrate that the cilium is necessary for the differentiation of APs into CAFs. BCCs increase production of TGF-β1 by APs, which is a known inducer of CAFs. Pharmacological inhibition of TGF-β1 signaling in APs prevents their conversion into CAFs. Since we previously showed that deletion of the APs’ cilium inhibits TGF-β1 signaling, we propose that BCCs induce TGF-β1 production in Aps, which binds to the primary cilium of Aps and leads to their differentiation into CAFs. Inhibition of APs conversion into CAFs induces a loss in some of the biological effects of CAFs since deletion of the cilium of APs decreases their effect on the migration of BCCs. This is the first observation of a function of the cilium of APs in their conversion into CAFs, and its consequences on BCCs.

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Section: Introductionmentioning

confidence: 99%

The Primary Cilium of Adipose Progenitors Is Necessary for Their Differentiation into Cancer-Associated Fibroblasts that Promote Migration of Breast Cancer Cells In Vitro

Peraldi

Ladoux

Giorgetti‐Peraldi

et al. 2020

Cells

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“…Growing evidence revealed that obesity promotes BC cells proliferation, migration, and invasion via modulating the levels of the adipokines secreted from obese ADSCs. 8,11,12,15 In the current study, we investigated the anti-proliferative activity of LG on obesity-associated BC. The impact of LG on modulating the adipokines in ADSCs and BC cells was also studied.…”

Section: Discussionmentioning

confidence: 99%

“…18 -20 Second, obesity alters the secretory profile of ADSCs to enhance cancer growth. 8,11,12,15,17 Compared to ADSCs isolated from lean women, ADSCs from obese subjects expressed significantly higher levels of leptin 8,12,15 and pro-inflammatory cytokines including IL-6, TNF-α, IL-12 and adhesion molecules. 11,21…”

Section: Introductionmentioning

confidence: 99%

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Anti-Proliferative Activity of Glucagon-Like Peptide-1 Receptor Agonist on Obesity-Associated Breast Cancer: The Impact on Modulating Adipokines’ Expression in Adipocytes and Cancer Cells

et al. 2021

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Obesity is associated with high risk and poor prognosis of breast cancer (BC). Obesity promotes BC cells proliferation via modulating the production of adipokines, including adiponectin (anti-neoplastic adipokine), leptin (carcinogenic adipokine) and inflammatory mediators. In the present study we investigated the anti-proliferative effects of liraglutide (LG; anti-diabetic and weight reducing drug) on MCF-7 human BC cells cultured in obese adipose tissue-derived stem cells-conditioned medium (ADSCs-CM) and whether this effect is mediated via modulating the adipokines in ADSCs and cancer cells. Proliferation was investigated using AlamarBlue viability test, colony forming assay and cell cycle analysis. Levels and expression of adipokines and their receptors were assayed using ELISA and RT-PCR. LG caused 48% inhibition of MCF-7 proliferation in obese ADSCs-CM, reduced the colony formation and induced G0/G1 phase arrest. LG also decreased the levels of inflammatory mediators, suppressed the expression of leptin, while increased mRNA levels of adiponectin and their receptors in obese ADSCs and cancer cells cultured in obese ADCSs-CM. In conclusion, LG could mitigate BC cell growth in obese subjects; therefore it could be used for clinical prevention and/or treatment of BC in obese subjects. It may assist to improve treatment outcomes and, reduce the mortality rate in obese patients with BC.

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“…In breast, mammary tissue is embedded in the adipose tissue, which allows direct paracrine action of adipose-derived factors on mammary epithelial cells; thereby the stromal cells contribute to the regulation of cellular growth and differentiation of the mammary gland (18). However, adipose tissue-derived cells may also be a source for tumor stroma (12), and their secreted growth factors, especially IGF1, contribute to the growth of breast cancer cells (19). In this way, ASCs may play crucial role in the development of breast cancer and in the relapse of the disease as well.…”

Section: Discussionmentioning

confidence: 99%

Polyploid Adipose Stem Cells Shift the Balance of IGF1/IGFBP2 to Promote the Growth of Breast Cancer

et al. 2020

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Background: The close proximity of adipose tissue and mammary epithelium predispose involvement of adipose cells in breast cancer development. Adipose-tissue stem cells (ASCs) contribute to tumor stroma and promote growth of cancer cells. In our previous study, we have shown that murine ASCs, which undergo polyploidization during their prolonged in vitro culturing, enhanced the proliferation of 4T1 murine breast cancer cells in IGF1 dependent manner.Aims: In the present study, our aim was to clarify the regulation of ASC-derived IGF1.Methods: 4T1 murine breast carcinoma cells were co-transplanted with visceral fat-derived ASCs (vASC) or with the polyploid ASC.B6 cell line into female BALB/c mice and tumor growth and lung metastasis were monitored. The conditioned media of vASCs and ASC.B6 cells were subjected to LC-MS/MS analysis and the production of IGFBP2 was verified by Western blotting. The regulatory effect was examined by adding recombinant IGFBP2 to the co-culture of ASC.B6 and 4T1. Akt/protein kinase B (PKB) activation was detected by Western blotting.Results: Polyploid ASCs promoted the tumor growth and metastasis more potently than vASCs with normal karyotype. vASCs produced the IGF1 regulator IGFBP2, which inhibited proliferation of 4T1 cells. Downregulation of IGFBP2 by polyploidization of ASCs and enhanced secretion of IGF1 allowed survival signaling in 4T1 cells, leading to Akt phosphorylation. Conclusions:Our results implicate that ASCs in the tumor microenvironment actively regulate the growth of breast cancer cells through the IGF/IGFBP system. Keywords: adipose stem cells, breast cancer, tumor stroma, insulin-like growth factor 1, insulin-like growth factor binding protein 2

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Adipose Stem Cells and Cancer: Concise Review

Cited by 25 publications

References 75 publications

The Primary Cilium of Adipose Progenitors Is Necessary for Their Differentiation into Cancer-Associated Fibroblasts that Promote Migration of Breast Cancer Cells In Vitro

The Primary Cilium of Adipose Progenitors Is Necessary for Their Differentiation into Cancer-Associated Fibroblasts that Promote Migration of Breast Cancer Cells In Vitro

Anti-Proliferative Activity of Glucagon-Like Peptide-1 Receptor Agonist on Obesity-Associated Breast Cancer: The Impact on Modulating Adipokines’ Expression in Adipocytes and Cancer Cells

Polyploid Adipose Stem Cells Shift the Balance of IGF1/IGFBP2 to Promote the Growth of Breast Cancer

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