Impact of Mesenchymal Stem Cell secreted PAI-1 on colon cancer cell migration and proliferation

Hogan, Niamh M.; Joyce, Myles R.; Murphy, Mary; Barry, Frank; O’Brien, Timothy; Kerin, Michael J.; Dwyer, Róisín M.

doi:10.1016/j.bbrc.2013.05.013

Cited by 42 publications

(36 citation statements)

References 25 publications

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“…In particular, growing evidence supports the hypothesis that BM-MSCs participate in TME differentiation into carcinoma-associated fibroblasts (CAFs) [ 21 , 22 ]. Many studies reported that BM-MSCs promote tumor proliferation and invasion of different carcinomas including breast [ 4 , 23 ], prostate [ 20 , 22 ], osteosarcoma [ 24 , 25 , 26 ] and colon [ 27 , 28 , 29 ]. Recent studies have also clarified the role of tumor cells as cells capable of modifying their environment by releasing important biomolecules from extracellular vesicles [ 7 ].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of AQP1 Hampers Osteosarcoma and Hepatocellular Carcinoma Progression Mediated by Bone Marrow-Derived Mesenchymal Stem Cells

Pelagalli

Nardelli

Fontanella

et al. 2016

IJMS

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The complex cross-talk between tumor cells and their surrounding stromal environment plays a key role in the pathogenesis of cancer. Among several cell types that constitute the tumor stroma, bone marrow-derived mesenchymal stem cells (BM-MSCs) selectively migrate toward the tumor microenvironment and contribute to the active formation of tumor-associated stroma. Therefore, here we elucidate the involvement of BM-MSCs to promote osteosarcoma (OS) and hepatocellular carcinoma (HCC) cells migration and invasion and deepening the role of specific pathways. We analyzed the function of aquaporin 1 (AQP1), a water channel known to promote metastasis and neoangiogenes. AQP1 protein levels were analyzed in OS (U2OS) and HCC (SNU-398) cells exposed to conditioned medium from BM-MSCs. Tumor cell migration and invasion in response to BM-MSC conditioned medium were evaluated through a wound healing assay and Boyden chamber, respectively. The results showed that the AQP1 level was increased in both tumor cell lines after treatment with BM-MSC conditioned medium. Moreover, BM-MSCs-mediated tumor cell migration and invasion were hampered after treatment with AQP1 inhibitor. These data suggest that the recruitment of human BM-MSCs into the tumor microenvironment might cause OS and HCC cell migration and invasion through involvement of AQP1.

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Section: Discussionmentioning

confidence: 99%

Inhibition of AQP1 Hampers Osteosarcoma and Hepatocellular Carcinoma Progression Mediated by Bone Marrow-Derived Mesenchymal Stem Cells

Pelagalli

Nardelli

Fontanella

et al. 2016

IJMS

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“…PAI-1 principally inhibits urokinase plasminogen activator (uPA), which acts as an inducer of fibrinolysis and extracellular matrix degradation [71]. PAI-1 expression is also associated with increased tumor cell invasion and metastasis [72], and some studies have shown that PAI-1 is a poor prognostic indicator for a number of cancers, including breast cancer and colon cancer [72,73]. While most of the studies to date have focused on adipose tissue as a whole, few studies have investigated the impact of obesity on the ASCs.…”

Section: Pai-1mentioning

confidence: 99%

Concise Review: The Obesity Cancer Paradigm: Exploration of the Interactions and Crosstalk with Adipose Stem Cells

et al. 2015

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With the recognition of obesity as a global health crisis, researchers have devoted greater effort to defining and understanding the pathophysiological molecular pathways regulating the biology of adipose tissue and obesity. Obesity, the excessive accumulation of adipose tissue due to hyperplasia and hypertrophy, has been linked to an increased incidence and aggressiveness of colon, hematological, prostate, and postmenopausal breast cancer cancers. The increased morbidity and mortality of obesity-associated cancers has been attributed to higher levels of hormones, adipokines, and cytokines secreted by the adipose tissue. The increased amount of adipose tissue also results in higher numbers of adipose stromal/stem cells (ASCs). These ASCs have been shown to impact cancer progression directly through several mechanisms, including the increased recruitment of ASCs to the tumor site and increased production of cytokines and growth factors by ASCs and other cells within the tumor stroma. Emerging evidence indicates that obesity induces alterations in the biologic properties of ASCs, subsequently leading to enhanced tumorigenesis and metastasis of cancer cells. This review will discuss the links between obesity and cancer tumor progression, including obesity-associated changes in adipose tissue, inflammation, adipokines and chemokines. Novel topics will include a discussion of the contribution of ASCs to this complex system with an emphasis on their role in the tumor stroma. The reciprocal and circular feedback loop between obesity and ASCs as well as the mechanisms by which ASCs from obese patients alter the biology of cancer cells and enhance tumorigenesis will be discussed.

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“…PAI-1, a well-established unfavorable prognostic factor in breast cancer (109), is a secretory protein able to promote cellular migration and angiogenesis (110,111). Since PAI-1 secreted by MSCs is able to enhance migratory activities of cancer cells (112) (Dittmer et al unpublished data), it is reasonable to assume that CSC-secreted PAI-1 may also affect cell motility.…”

Section: Paracrine Effects Of Stem Cells In Cancermentioning

confidence: 99%

Paracrine effects of stem cells in wound healing and cancer progression

Dittmer¹,

Leyh²

2014

International Journal of Oncology

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Stem cells play an important role in tissue repair and cancer development. The capacity to self-renew and to differentiate to specialized cells allows tissue-specific stem cells to rebuild damaged tissue and cancer stem cells to initiate and promote cancer. Mesenchymal stem cells, attracted to wounds and cancer, facilitate wound healing and support cancer progression primarily by secreting bioactive factors. There is now growing evidence that, like mesenchymal stem cells, also tissue-specific and cancer stem cells manipulate their environment by paracrine actions. Soluble factors and microvesicles released by these stem cells have been shown to protect recipient cells from apoptosis and to stimulate neovascularization. These paracrine mechanisms may allow stem cells to orchestrate wound healing and cancer progression. Hence, understanding these stem cell-driven paracrine effects may help to improve tissue regeneration and cancer treatment.

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Impact of Mesenchymal Stem Cell secreted PAI-1 on colon cancer cell migration and proliferation

Cited by 42 publications

References 25 publications

Inhibition of AQP1 Hampers Osteosarcoma and Hepatocellular Carcinoma Progression Mediated by Bone Marrow-Derived Mesenchymal Stem Cells

Inhibition of AQP1 Hampers Osteosarcoma and Hepatocellular Carcinoma Progression Mediated by Bone Marrow-Derived Mesenchymal Stem Cells

Concise Review: The Obesity Cancer Paradigm: Exploration of the Interactions and Crosstalk with Adipose Stem Cells

Paracrine effects of stem cells in wound healing and cancer progression

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