VEGF-A promotes lymphoma tumour growth by activation of STAT proteins and inhibition of p27KIP1 via paracrine mechanisms

Roorda, Berber D.; Elst, Arja ter; Scherpen, Frank J.G.; Boer, Tiny G. J. Meeuwsen–de; Kamps, Willem A.; Bont, Eveline S.J.M. de

doi:10.1016/j.ejca.2009.12.027

Cited by 14 publications

(11 citation statements)

References 34 publications

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“…Cyclin-dependent kinase (CDK) inhibitors, including p21, p27 and p15/p15 INK45 , could regulate cell cycles by inhibiting cyclin and CDK activity, thus resulting in G1 arrest. [18][19][20][21][22][23] The activation of PPAR-g could control the cell cycle by regulating p27. The results were confirmed in our study, as 18a-GA decreased cyclin D1 but increased p27 levels.…”

Section: Discussionmentioning

confidence: 99%

18α‐glycyrrhetinic acid extracted from Glycyrrhiza radix inhibits proliferation and promotes apoptosis of the hepatic stellate cell line

Zong

Qu²,

Xu³

et al. 2013

J of Digest Diseases

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Section: Discussionmentioning

confidence: 99%

18α‐glycyrrhetinic acid extracted from Glycyrrhiza radix inhibits proliferation and promotes apoptosis of the hepatic stellate cell line

Zong

Qu²,

Xu³

et al. 2013

J of Digest Diseases

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“…Hence, it is possible that ERM-mediated membrane structures regulate tumor microenvironment by providing nutrient/information exchange between cells, as well as secretion of cell survival factors such as cytokines and growth factors. In fact, a high circulating level of vascular endothelial growth factor A (VEGF-A) has been detected in patients with non-Hodgkin’s lymphoma, and tumor cells were identified as the producers of this growth factor in vivo (103). VEGF-A promotes tumor growth by stimulating tumor stromal cells to secret various cytokines including IL-4, IL-6 and IL-10, leading to paracrine activation of tumor cells (103), as well as stimulates cancer cell metastasis by upregulation and activation of ERM family proteins moesin through RhoA/ROCK-2 pathway (104).…”

Section: Erm Proteins In Germinal Center Biologymentioning

confidence: 99%

“…In fact, a high circulating level of vascular endothelial growth factor A (VEGF-A) has been detected in patients with non-Hodgkin’s lymphoma, and tumor cells were identified as the producers of this growth factor in vivo (103). VEGF-A promotes tumor growth by stimulating tumor stromal cells to secret various cytokines including IL-4, IL-6 and IL-10, leading to paracrine activation of tumor cells (103), as well as stimulates cancer cell metastasis by upregulation and activation of ERM family proteins moesin through RhoA/ROCK-2 pathway (104). VEGF is also important for angiogenesis, and hence accelerates metastasis of tumor cells to lymph nodes and distant organs (105).…”

Section: Erm Proteins In Germinal Center Biologymentioning

confidence: 99%

The Ezrin-Radixin-Moesin Family of Proteins in the Regulation of B-Cell Immune Response

Pore

Gupta

2015

Crit Rev Immunol

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Dynamic reorganization of the cortical cytoskeleton is essential for numerous cellular processes including B and T cell activation and migration. The Ezrin, Radixin and Moesin (ERM) family proteins play structural and regulatory roles in the rearrangement of plasma membrane flexibility and protrusions through their reversible interaction with cortical actin filaments and plasma membrane. Recent studies demonstrate that ERM proteins are not only involved in cytoskeletal organization but also offer a platform for the transmission of signals in response to a variety of extracellular stimuli through their ability to crosslink transmembrane receptors with downstream signaling components. In this review, we summarize the present knowledge and recent progress made towards elucidating a novel role of ERM proteins in the regulation of B function in health and disease.

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“…However, high vascularity was found in the bone marrow of children with acute lymphoblastic leukemia and a positive correlation between the hemangiogenic protein Vascular Endothelial Growth Factor-A (VEGF-A) and lymphoma progression has been observed [12,13]. Lymphangiogenic growth factors, most importantly VEGF-C and VEGF-D [14-16], increase the number of lymph node metastases of numerous carcinomas [17].…”

Section: Introductionmentioning

confidence: 99%

Specific tumor-stroma interactions of EBV-positive Burkitt's lymphoma cells in the chick chorioallantoic membrane

et al. 2012

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BackgroundBurkitt's lymphoma (BL) is an aggressive Non-Hodgkin lymphoma. Epstein-Barr Virus (EBV) is able to transform B cells and is a causative infectious agent in BL. The precise role of EBV in lymphoma progression is still unclear. Most investigations have concentrated on cell autonomous functions of EBV in B cells. Functions of the local environment in BL progression have rarely been studied, mainly due to the lack of appropriate in vivo models. Therefore, we inoculated different human BL cell-lines onto the chorioallantoic membrane (CAM) of embryonic day 10 (ED10) chick embryos and re-incubated until ED14 and ED17.ResultsAll cell-lines formed solid tumors. However, we observed strong differences in the behavior of EBV+ and EBV- cell-lines. Tumor borders of EBV+ cells were very fuzzy and numerous cells migrated into the CAM. In EBV- tumors, the borders were much better defined. In contrast to EBV- cells, the EBV+ cells induced massive immigration of chick leukocytes at the tumor borders and the development of granulation tissue with large numbers of blood vessels and lymphatics, although the expression of pro- and anti-angiogenic forms of Vascular Endothelial Growth Factors/receptors was the same in all BL cell-lines tested. The EBV+ cell-lines massively disseminated via the lymphatics and completely occluded them.ConclusionsOur data suggest that the EBV+ cells attract pro-angiogenic leukocytes, which then induce secondary tumor-stroma interactions contributing to the progression of BL. We show that the CAM is a highly suitable in vivo model to study the differential behavior of BL cell-lines.

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VEGF-A promotes lymphoma tumour growth by activation of STAT proteins and inhibition of p27KIP1 via paracrine mechanisms

Cited by 14 publications

References 34 publications

18α‐glycyrrhetinic acid extracted from Glycyrrhiza radix inhibits proliferation and promotes apoptosis of the hepatic stellate cell line

18α‐glycyrrhetinic acid extracted from Glycyrrhiza radix inhibits proliferation and promotes apoptosis of the hepatic stellate cell line

The Ezrin-Radixin-Moesin Family of Proteins in the Regulation of B-Cell Immune Response

Specific tumor-stroma interactions of EBV-positive Burkitt's lymphoma cells in the chick chorioallantoic membrane

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