Effects of SEMA3G on migration and invasion of glioma cells

Zhou, Xiuping; Ma, Lin; Li, Jian; Gu, Jiafeng; Shi, Qiong; Yu, Rong

doi:10.3892/or.2012.1796

Cited by 22 publications

(16 citation statements)

References 37 publications

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“…Overexpression of VGF inhibits colony formation of ovarian cancer cells, however, VGF promoter hypermethylation correlates with better patient survival [72]. In contrast to our results, SEMA3G inhibits cell migration and invasion in glioma [73]. SLC5A1 promotes growth and proliferation of pancreatic cancer [74].…”

Section: Discussioncontrasting

confidence: 88%

Downstream Effectors of ILK in Cisplatin-Resistant Ovarian Cancer

Reyes-González

Quiñones-Díaz

Santana

et al. 2020

Cancers

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Despite good responses to first-line treatment with platinum-based combination chemotherapy, most ovarian cancer patients will relapse and eventually develop platinum-resistant disease with poor prognosis. Although reports suggest that integrin-linked kinase (ILK) is a potential target for ovarian cancer treatment, identification of ILK downstream effectors has not been fully explored. The purpose of this study was to investigate the molecular and biological effects of targeting ILK in cisplatin-resistant ovarian cancer. Western blot analysis showed that phosphorylation levels of ILK were higher in cisplatin-resistant compared with cisplatin-sensitive ovarian cancer cells. Further immunohistochemical analysis of ovarian cancer patient samples showed a significant increase in phosphorylated ILK levels in the tumor tissue when compared to normal ovarian epithelium. Targeting ILK by small-interfering RNA (siRNA) treatment reduced cisplatin-resistant cell growth and invasion ability, and increased apoptosis. Differential gene expression analysis by RNA sequencing (RNA-Seq) upon ILK-siRNA transfection followed by Ingenuity Pathway Analysis (IPA) and survival analysis using the Kaplan–Meier plotter database identified multiple target genes involved in cell growth, apoptosis, invasion, and metastasis, including several non-coding RNAs. Taken together, results from this study support ILK as an attractive target for ovarian cancer and provide potential ILK downstream effectors with prognostic and therapeutic value.

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Section: Discussioncontrasting

confidence: 88%

Downstream Effectors of ILK in Cisplatin-Resistant Ovarian Cancer

Reyes-González

Quiñones-Díaz

Santana

et al. 2020

Cancers

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“…SLIT/ROBO signaling, canonically involved in axon pathfinding as a chemorepulsive ligand-receptor system (Brose et al, 1999; Kidd et al, 1999), functions similarly as a chemorepellant in glioma (Mertsch et al, 2008). Semaphorins function chiefly as short-range inhibitory signals for developing axons, and HGGs express both semaphorins and the receptors plexins and neuropilins (Rieger et al, 2003); semaphorin signaling has been found to limit glioma motility (Li and Lee, 2010; Zhou et al, 2012). …”

Section: Discussionmentioning

confidence: 99%

Neural Precursor-Derived Pleiotrophin Mediates Subventricular Zone Invasion by Glioma

Qin

Cooper

Abbott

et al. 2017

Cell

167

148

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Summary The lateral ventricle subventricular zone (SVZ) is a frequent and consequential site of pediatric and adult glioma spread, but the cellular and molecular mechanisms mediating this are poorly understood. We demonstrate that neural precursor cell (NPC):glioma cell communication underpins this propensity of glioma to colonize the SVZ through secretion of chemoattractant signals toward which glioma cells home. Biochemical, proteomic, and functional analyses of SVZ NPC-secreted factors revealed the neurite outgrowth-promoting factor pleiotrophin, along with required binding partners SPARC/SPARCL1 and HSP90B, as key mediators of this chemoattractant effect. Pleiotrophin expression is strongly enriched in the SVZ, and pleiotrophin knockdown starkly reduced glioma invasion of the SVZ in the murine brain. Pleiotrophin, in complex with the binding partners, activated glioma Rho/ROCK signaling, and ROCK inhibition decreased invasion toward SVZ NPC-secreted factors. These findings demonstrate a pathogenic role for NPC:glioma interactions and potential therapeutic targets to limit glioma invasion.

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“… 249 SEMA3G also prevents migration and invasion in an autocrine and paracrine fashion by inhibiting the activity of MMP2 in vitro, and inhibits tumor growth in an orthotopic model of GBM. 219 , 250 …”

Section: Structure Signaling and Function Of Class 3 Semaphorins Anmentioning

confidence: 99%

The emerging role of class-3 semaphorins and their neuropilin receptors in oncology

Nasarre¹,

Gemmill²,

Drabkin³

2014

OTT

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The semaphorins, discovered over 20 years ago, are a large family of secreted or transmembrane and glycophosphatidylinositol -anchored proteins initially identified as axon guidance molecules crucial for the development of the nervous system. It has now been established that they also play important roles in organ development and function, especially involving the immune, respiratory, and cardiovascular systems, and in pathological disorders, including cancer. During tumor progression, semaphorins can have both pro- and anti-tumor functions, and this has created complexities in our understanding of these systems. Semaphorins may affect tumor growth and metastases by directly targeting tumor cells, as well as indirectly by interacting with and influencing cells from the micro-environment and vasculature. Mechanistically, semaphorins, through binding to their receptors, neuropilins and plexins, affect pathways involved in cell adhesion, migration, invasion, proliferation, and survival. Importantly, neuropilins also act as co-receptors for several growth factors and enhance their signaling activities, while class 3 semaphorins may interfere with this. In this review, we focus on the secreted class 3 semaphorins and their neuropilin co-receptors in cancer, including aspects of their signaling that may be clinically relevant.

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Effects of SEMA3G on migration and invasion of glioma cells

Cited by 22 publications

References 37 publications

Downstream Effectors of ILK in Cisplatin-Resistant Ovarian Cancer

Downstream Effectors of ILK in Cisplatin-Resistant Ovarian Cancer

Neural Precursor-Derived Pleiotrophin Mediates Subventricular Zone Invasion by Glioma

The emerging role of class-3 semaphorins and their neuropilin receptors in oncology

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