Differential expression of neuropilin-1 in malignant and benign prostatic stromal tissue

Vanveldhuizen, Peter J.; Zulfiqar, Muhammad; Banerjee, Snigdha; Cherian, Rachel; Saxena, Neela K.; Rabe, Amy; Thrasher, J. Brantley

doi:10.3892/or.10.5.1067

Cited by 32 publications

(33 citation statements)

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“…Accumulating evidence suggests that neuropilin-1 is overexpressed in several cancers and its high expression is correlated with poor prognosis (Ding et al, 2000;Kawakami et al, 2002;Roche et al, 2002;Vanveldhuizen et al, 2003;Broholm and Laursen, 2004;Fukahi et al, 2004;Li et al, 2004;Osada et al, 2004;Parikh et Figure 8 Semaphorin3A (Sema3A) expression in human glioblastoma multiformes (GBMs). (a) Immunohistochemical analysis of Sema3A in human GBM tissue.…”

Section: Discussionmentioning

confidence: 99%

Autocrine semaphorin 3A signaling promotes glioblastoma dispersal

et al. 2009

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Glioblastoma multiforme (GBM) is the most malignant glioma type with diffuse borders due to extensive tumor cell infiltration. Therefore, understanding the mechanism of GBM cell dispersal is critical for developing effective therapies to limit infiltration. We identified neuropilin-1 as a mediator of cancer cell invasion by a functional proteomic screen and showed its role in GBM cells. Neuropilin-1 is a receptor for semaphorin3A (Sema3A), a secreted chemorepellent that facilitates axon guidance during neural development. Although neuropilin-1 expression in GBMs was previously shown, its role as a Sema3A receptor remained elusive. Using fluorophore-assisted light inactivation and RNA interference , we showed that neuropilin-1 is required for GBM cell migration. We also showed that GBM cells secrete Sema3A endogenously, and RNA interferencemediated downregulation of Sema3A inhibits migration and alters cell morphology that is dependent on Rac1 activity. Sema3A depletion also reduces dispersal, which is recovered by supplying Sema3A exogenously. Extracellular application of Sema3A decreases cell-substrate adhesion in a neuropilin-1-dependent manner. Using immunohistochemistry, we showed that Sema3A is overexpressed in a subset of human GBMs compared with the non-neoplastic brain. Together, these findings implicate Sema3A as an autocrine signal for neuropilin-1 to promote GBM dispersal by modulating substrate adhesion and suggest that targeting Sema3A-neuropilin-1 signaling may limit GBM infiltration.

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Section: Discussionmentioning

confidence: 99%

Autocrine semaphorin 3A signaling promotes glioblastoma dispersal

et al. 2009

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“…The NRP-1 is a transmembrane receptor glycoprotein whose expression is known to be increased during the progression of breast, prostate, and lung tumors (Soker et al, 1998;Stephenson et al, 2002;Lantuejoul et al, 2003;Vanveldhuizen et al, 2003). The NRP-1 serves as a vascular endothelial growth factor (VEGF) coreceptor and enhances VEGF receptor 2 (VEGFR2)/kinase insert domain-containing receptor (KDR) binding, tumor angiogenesis, and progression (Soker et al, 1998;Miao et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Cigarette smoke condensate-induced transformation of normal human breast epithelial cells in vitro

et al. 2004

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In the present study, we showed that a single-dose treatment of normal breast epithelial cell line, MCF10A, for 72 h with cigarette smoke condensate (CSC) resulted in a transformed phenotype. The anchorage-dependent growth of these cells was decreased due to increased cell cycle arrest in S-G 2 /M phase; however, the surviving cells developed resistance due to an increased Bcl-xL to Bax ratio. Levels of PCNA and gadd45 proteins -involved in DNA repair in response to genomic damage -were increased, suggesting that the cells were responding to CSC-induced genomic damage. The transformation of MCF10A cells was determined by their colony-forming efficiency in soft-agar in an anchorage-independent manner. CSC-treated MCF10A cells efficiently formed colonies in soft-agar. We then re-established cell lines from the soft-agar colonies and further examined the persistence of their transforming characteristics. The reestablished cell lines, when plated after 17 passages without CSC treatment, still formed colonies in the softagar. An increased staining of neuropilin-1 (NRP-1) further showed a transformation characteristic of MCF10A cells treated with CSC. In summary, our results suggest that CSC is capable of transforming the MCF10A cells in vitro, supporting the role of cigarette smoking and increased risk for breast cancer.

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“…130 They are expressed on different types of tumor cells, 131 and tumor NRP1 levels correlate with advanced disease and prognosis in certain cancers, such as prostate and lung cancer. [132][133][134] A preclinical study indicates that a monoclonal antibody blocking the binding of VEGF to NRP1 (αNRP1 VEGF ) inhibits tumor growth. Upon combination with anti-VEGF, tumor growth was inhibited more, 131,135 raising the question whether αNRP1 VEGF may perhaps inhibit other ligands, such as PlGF, HGF, FGFs, and so on.…”

Section: Inhibiting Vessel Maturation or Lymphangiogenesis By Blockinmentioning

confidence: 99%

Mechanisms of Resistance to Anti-Angiogenic Therapy and Development of Third-Generation Anti-Angiogenic Drug Candidates

Loges¹,

Schmidt²,

2010

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The concept of inhibiting tumor neovessels has taken the hurdle from the bench to the bedside and now represents an extra pillar of anticancer treatment. So far, anti-angiogenic therapy prolongs survival in the order of months in some settings while failing to induce a survival benefit in others, in part because of intrinsic refractoriness or evasive escape. This review provides an update on recent mechanisms via which tumor and stromal cells induce resistance and discusses recent evolutions in the (pre)clinical development of novel third-generation anti-angiogenic agents to overcome this problem.

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Differential expression of neuropilin-1 in malignant and benign prostatic stromal tissue

Cited by 32 publications

References 0 publications

Autocrine semaphorin 3A signaling promotes glioblastoma dispersal

Autocrine semaphorin 3A signaling promotes glioblastoma dispersal

Cigarette smoke condensate-induced transformation of normal human breast epithelial cells in vitro

Mechanisms of Resistance to Anti-Angiogenic Therapy and Development of Third-Generation Anti-Angiogenic Drug Candidates

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