Adipose derived stem cells isolated from omentum: A novel source of chemokines for ovarian cancer growth

Rezaeifard, Somayeh; Razmkhah, Mahboobeh; Robati, Minoo; Momtahan, Mozhdeh; Ghaderi, Abbas

doi:10.4103/0973-1482.131451

Cited by 7 publications

(6 citation statements)

References 32 publications

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“…The pro-growth effects of BMSCs on cancer have been widely demonstrated [ 31 - 33 ]. Recent reports led to similar conclusions that ADSCs promoted cancer growth and metastasis [ 8 - 11 ]. Moreover, Eterno et al found that ADSCs could enhance breast tumor self-renewal and facilitate breast cancer recurrence via HGF/c-Met axis [ 21 ].…”

Section: Discussionmentioning

confidence: 71%

“…Although current knowledge of the biological impacts of MSCs on tumor development is greatly improved, the underlying effects of MSCs from different origins remain controversial. Accumulating evidence indicates that ADSCs promote the tumor growth and metastasis of various cancers [ 8 - 11 ], whereas conflicting reports reveal the anti-tumorigenic potentials of ADSCs such as anti-proliferation and pro-apoptosis [ 12 - 14 ]. Hence, the elusive role of ADSCs in tumor development causes the safety concerns in clinical utilization.…”

Section: Introductionmentioning

confidence: 99%

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Adipose-derived stem cells promote tumor initiation and accelerate tumor growth by interleukin-6 production

Wei

Zeng

et al. 2015

Oncotarget

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Adipose-derived stem cells (ADSCs) are multipotent cells that have attracted much recent attention. Here, we show that ADSCs enhance sphere formation and in vivo tumor initiation of breast and colon cancer cells. In co-culture, ADSCs induced several stem cell markers in cancer cells. ADSCs also accelerated tumor growth. Interaction of ADSCs and cancer cells stimulated secretion of interlukin-6 in ADSCs, which in turn acted in a paracrine manner on cancer cells to enhance their malignant properties. Interleukin-6 regulated stem cell-related genes and activated JAK2/STAT3 in cancer cells. We suggest that ADSCs may enhance tumor initiation and promotion.

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Section: Discussionmentioning

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Adipose-derived stem cells promote tumor initiation and accelerate tumor growth by interleukin-6 production

Wei

Zeng

et al. 2015

Oncotarget

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“…The role of IP-10 (CXCL-10) has not been well studied in relation to progression of gliomas. However, a recent study by Rezaeifard et al [ 74 ] has implicated adipose stem cell derived IP-10 in the pathogenesis of ovarian cancer. Further studies in this direction may provide valuable insight into alternative or additional mechanisms by which IL-17–IL-17R interaction could promote GSC stimulation and glioma progression.…”

Section: Discussionmentioning

confidence: 99%

Preferential expression of functional IL-17R in glioma stem cells: potential role in self-renewal

et al. 2016

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Gliomas are the most common primary brain tumor and one of the most lethal solid tumors. Mechanistic studies into identification of novel biomarkers are needed to develop new therapeutic strategies for this deadly disease. The objective for this study was to explore the potential direct impact of IL-17−IL-17R interaction in gliomas. Immunohistochemistry and flow cytometry analysis of 12 tumor samples obtained from patients with high grade gliomas revealed that a considerable population (2–19%) of cells in all malignant gliomas expressed IL-17RA, with remarkable co-expression of the glioma stem cell (GSC) markers CD133, Nestin, and Sox2. IL-17 enhanced the self-renewal of GSCs as determined by proliferation and Matrigel® colony assays. IL-17 also induced cytokine/chemokine (IL-6, IL-8, interferon-γ-inducible protein [IP-10], and monocyte chemoattractant protein-1 [MCP-1]) secretion in GSCs, which were differentially blocked by antibodies against IL-17R and IL-6R. Western blot analysis showed that IL-17 modulated the activity of signal transducer and activator of transcription 3 (STAT3), nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB), glycogen synthase kinase-3β (GSK-3β) and β-catenin in GSCs. While IL-17R-mediated secretion of IL-6 and IL-8 were significantly blocked by inhibitors of NF-κB and STAT3; NF-κB inhibitor was more potent than STAT3 inhibitor in blocking IL-17-induced MCP-1 secretion. Overall, our results suggest that IL-17–IL-17R interaction in GSCs induces an autocrine/paracrine cytokine feedback loop, which may provide an important signaling component for maintenance/self-renewal of GSCs via constitutive activation of both NF-κB and STAT3. The results also strongly implicate IL-17R as an important functional biomarker for therapeutic targeting of GSCs.

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“…Over the years, ADSCs have gained increasing attention for their role in supporting tumor growth and progression [51]. Many authors have demonstrated that ADSCs, and particularly those from omental adipose tissue, can increase ovarian cancer cell proliferation and promote a shift toward a more aggressive, invasive, and metastatic phenotype [10,31,52,53] (Figure 2). taxane-induced cell death.…”

Section: Adscs In the Ovarian Cancer Microenvironmentmentioning

confidence: 99%

“…ADSCs are attracted to the tumor site and have a specific tumor homing due to several chemotactic factors in the tumor microenvironment. In particular, in the omentum of ovarian cancer patients, high levels of CXCL-10 and CCR5 have been described [53]. Furthermore, recruited ADSCs secreted IL-10, which has a strong chemotactic activity for Treg lymphocytes and could play a role in immunosuppression in the tumor microenvironment.…”

Section: The Effects Of Tumor Cells On Adsc Recruitment and Adsc Phenotypic Changesmentioning

confidence: 99%

Mesenchymal Stem Cells in Adipose Tissue and Extracellular Vesicles in Ovarian Cancer Patients: A Bridge toward Metastatic Diffusion or a New Therapeutic Opportunity?

Storti

Kim

Terriaca

et al. 2021

Cells

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Ovarian cancer is one of the deadliest malignancies among women. Approximately 75% of the patients with ovarian cancer are diagnosed with advanced disease that already has metastasis, particularly to the omentum. The omentum constitutes the ideal soil for ovarian cancer metastasis due to a complex intraperitoneal milieu that favors and supports the whole metastatic process. Adipose-derived stem/stromal cells (ADSCs) are part of this microenvironment and foster tumor progression via sustained paracrine secretion, including extracellular vesicles (EVs). Nonetheless, the preferential relationship between ADSCs, ADSC-derived EVs, and ovarian cancer cells could be exploited to use ADSCs and EVs as a vehicle for anti-cancer therapies. This review will analyze the strict relations between tumor progression, metastatic disease, and adipose tissue with its staminal components. In addition, we will describe the crosstalk and biologic relationship between ADSCs and tumor cells, the role of EVs in intercellular communication, the establishment of drug resistance, metastatic capacity, and ovarian cancer progression. We will analyze the new therapeutic opportunities in treating ovarian cancer offered by ADSCs and EVs as a vehicle for therapeutic molecules to target precisely tumor cells and limit the systemic adverse effects. Finally, we will discuss the limitations of these therapeutic approaches.

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Adipose derived stem cells isolated from omentum: A novel source of chemokines for ovarian cancer growth

Abstract: Omental adipose tissue may play crucial roles for tumor promotion through the expression of tumor promoting chemokines. Accordingly, tumor surrounding adipose tissue may be a novel target for immunotherapy of cancer.

Cited by 7 publications

References 32 publications

Adipose-derived stem cells promote tumor initiation and accelerate tumor growth by interleukin-6 production

Adipose-derived stem cells promote tumor initiation and accelerate tumor growth by interleukin-6 production

Preferential expression of functional IL-17R in glioma stem cells: potential role in self-renewal

Mesenchymal Stem Cells in Adipose Tissue and Extracellular Vesicles in Ovarian Cancer Patients: A Bridge toward Metastatic Diffusion or a New Therapeutic Opportunity?

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