Overexpression of Nogo receptor 3 (NgR3) correlates with poor prognosis and contributes to the migration of epithelial cells of nasopharyngeal carcinoma patients

He, Jiangyi; Han, Ping; Liu, Yongdong; Song, Shi‐Jian; Feng, Guokai; An, Yu; Zhou, Anni; Wang, Hongbo; Li, Yuan; Lin, Zhi-Rui; Xia, Tian-Liang; Li, Manzhi; Liu, Yanmin; Huang, Xiaoming; Zhang, Hua; Zhong, Qian

doi:10.1007/s00109-017-1618-1

Cited by 9 publications

(12 citation statements)

References 70 publications

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“…Indeed, Jin et al (2016) demonstrated that Nogo-A was able to inhibit the migration and invasion of human malignant glioma cells via the downregulation of RhoA-cofilin signaling. On the contrary, NgR3 seems to induce nasopharyngeal carcinoma cell migration by activating focal adhesion kinase (FAK) ( He et al, 2018 ).…”

Section: Structure Of P75 Ntr and Binding Partnersmentioning

confidence: 99%

From Neural Crest Development to Cancer and Vice Versa: How p75NTR and (Pro)neurotrophins Could Act on Cell Migration and Invasion?

Wislet

Vandervelden

Rogister

2018

Front. Mol. Neurosci.

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The p75 neurotrophin receptor (p75NTR), also known as low-affinity nerve growth factor, belongs to the tumor necrosis factor family of receptors. p75NTR is widely expressed in the nervous system during the development, as well as, in the neural crest population, since p75NTR has been described as ubiquitously expressed and considered as a neural crest marker. Neural crest cells (NCCs) constitute an transient population accurately migrating and invading, with precision, defined sites of the embryo. During migration, NCCs are guided along distinct migratory pathways by specialized molecules present in the extracellular matrix or on the surfaces of those cells. Two main processes direct NCC migration during the development: (1) an epithelial-to-mesenchymal transition and (2) a process known as contact inhibition of locomotion. In adults, p75NTR remains expressed by NCCs and has been identified in an increasing number of cancer cells. Nonetheless, the regulation of the expression of p75NTR and the underlying mechanisms in stem cell biology or cancer cells have not yet been sufficiently addressed. The main objective of this review is therefore to analyze elements of our actual knowledge regarding p75NTR roles during the development (mainly focusing on neural crest development) and see how we can transpose that information from development to cancer (and vice versa) to better understand the link between p75NTR and cell migration and invasion. In this review, we successively analyzed the molecular mechanisms of p75NTR when it interacts with several coreceptors and/or effectors. We then analyzed which signaling pathways are the most activated or linked to NCC migration during the development. Regarding cancer, we analyzed the described molecular pathways underlying cancer cell migration when p75NTR was correlated to cancer cell migration and invasion. From those diverse sources of information, we finally summarized potential molecular mechanisms underlying p75NTR activation in cell migration and invasion that could lead to new research areas to develop new therapeutic protocols.

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Section: Structure Of P75 Ntr and Binding Partnersmentioning

confidence: 99%

From Neural Crest Development to Cancer and Vice Versa: How p75NTR and (Pro)neurotrophins Could Act on Cell Migration and Invasion?

Wislet

Vandervelden

Rogister

2018

Front. Mol. Neurosci.

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“…The pathogenesis of NPC is complicated, including the Epstein-Barr virus (EBV) infection, carcinogen hazards and individual susceptibility (1,4). In clinic, NPC exhibits low differentiation and high rates of metastasis compared with other types of cancers (5)(6)(7). Although chemotherapy and radiotherapy are used, the treatment efficacy for NPC is still unsatisfactory due to the local recurrence and distant metastasis (5,8).…”

Section: Introductionmentioning

confidence: 99%

“…In clinic, NPC exhibits low differentiation and high rates of metastasis compared with other types of cancers (5)(6)(7). Although chemotherapy and radiotherapy are used, the treatment efficacy for NPC is still unsatisfactory due to the local recurrence and distant metastasis (5,8). Therefore, it is important to understand the molecular mechanisms of NPC.…”

Section: Introductionmentioning

confidence: 99%

Effects of KIF2A on the prognosis of nasopharyngeal carcinoma and nasopharyngeal carcinoma cells

Zhang

Liu

et al. 2019

Oncol Lett

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Nasopharyngeal carcinoma (NPC) is a common tumor in south China. Kinesin family member 2A (KIF2A) belongs to the kinesin-13 family and is associated with the growth and invasion of a number of different types of human cancer, including ovarian, breast and prostate cancer. The aim of the present study was to evaluate the expression of KIF2A in NPC and explore the relationship between KIF2A and the basic characteristics of 5-8F cells. Immunohistochemistry was performed on tissues from 97 patients with NPC to assess KIF2A protein expression. KIF2A was knocked down by a specific short interfering (si)RNA in 5-8F cell lines. Cell proliferation, apoptosis and cycle were analyzed by MTT assay and flow cytometry. The invasive ability and angiogenesis were evaluated by Matrigel assay and reverse transcription-quantitative PCR. The level of KIF2A was associated with the growth and migration of primary tumor, nodal status and tumor stage. The viability of KIF2A-knockdown cells was decreased compared with that of the control cells. The number of apoptotic cells, as well as the percentage of cells in the G0/G1 phase, was higher in the KIF2A siRNA group compared with the control group. The invasive and angiogenetic ability of 5-8F cells in the KIF2A siRNA group was decreased compared with the control group. In conclusion, the expression of KIF2A correlated with the poor clinicopathological features in NPC. Therefore, KIF2A may serve an important role in the progression of NPC and proliferation of 5-8F cells, which might present a potential therapeutic target for patients with NPC.

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“…The cell surface receptors NG1 (RTN4R) and NG3 (RTN4RL1) also interact directly with specific CS‐GAGs, and CS‐E has been shown to compete for NG1 and NG3 binding (26). Over‐expression of NG3 has been linked to poor prognosis and increased metastasis in other cancers (60). Treating F98 cells with surfen significantly reduced expression of multiple CSPG receptor proteins, including LAR and RAGE.…”

Section: Discussionmentioning

confidence: 99%

Surfen‐mediated blockade of extratumoral chondroitin sulfate glycosaminoglycans inhibits glioblastoma invasion

Logun

Wynens

Simchick³

et al. 2019

The FASEB Journal

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Invasive spread of glioblastoma (GBM) is linked to changes in chondroitin sulfate (CS) proteoglycan (CSPG)‐associated sulfated glycosaminoglycans (GAGs) that are selectively up‐regulated in the tumor microenvironment (TME). We hypothesized that inhibiting CS‐GAG signaling in the TME would stem GBM invasion. Rat F98 GBM cells demonstrated enhanced preferential cell invasion into oversulfated 3‐dimensional composite of CSA and CS‐E [4‐ and 4,6‐sulfated CS‐GAG (COMP)] matrices compared with monosulfated (4‐sulfated) and unsulfated hyaluronic acid matrices in microfluidics‐based choice assays, which is likely influenced by differential GAG receptor binding specificities. Both F98 and human patient‐derived glioma stem cells (GSCs) demonstrated a high degree of colocalization of the GSC marker CD133 and CSPGs. The small molecule sulfated GAG antagonist bis‐2‐methyl‐4‐amino‐quinolyl‐6‐carbamide (surfen) reduced invasion and focal adhesions in F98 cells encapsulated in COMP matrices and blocked CD133 and antichondroitin sulfate antibody (CS‐56) detection of respective antigens in F98 cells and human GSCs. Surfen‐treated F98 cells down‐regulated CSPG‐binding receptor transcripts and protein, as well as total and activated ERK and protein kinase B. Lastly, rats induced with frontal lobe tumors and treated with a single intratumoral dose of surfen demonstrated reduced tumor burden and spread compared with untreated controls. These results present a first demonstration of surfen as an inhibitor of sulfated GAG signaling to stem GBM invasion.—Logun, M. T., Wynens, K. E., Simchick, G., Zhao, W., Mao, L., Zhao, Q., Mukherjee, S., Brat, D. J., Karumbaiah, L. Surfen‐mediated blockade of extratumoral chondroitin sulfate glycosaminoglycans inhibits glioblastoma invasion. FASEB J. 33, 11973‐11992 (2019). http://www.fasebj.org

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Overexpression of Nogo receptor 3 (NgR3) correlates with poor prognosis and contributes to the migration of epithelial cells of nasopharyngeal carcinoma patients

Cited by 9 publications

References 70 publications

From Neural Crest Development to Cancer and Vice Versa: How p75NTR and (Pro)neurotrophins Could Act on Cell Migration and Invasion?

From Neural Crest Development to Cancer and Vice Versa: How p75NTR and (Pro)neurotrophins Could Act on Cell Migration and Invasion?

Effects of KIF2A on the prognosis of nasopharyngeal carcinoma and nasopharyngeal carcinoma cells

Surfen‐mediated blockade of extratumoral chondroitin sulfate glycosaminoglycans inhibits glioblastoma invasion

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