Neuropilin 1 (NRP1) is a novel tumor marker in hepatocellular carcinoma

Lin, Jie; Zhang, Yingwei; Wu, Jugang; Li, Li; Chen, Ning; Ni, Peihong; Song, Lihua; Liu, Xiangfan

doi:10.1016/j.cca.2018.06.046

Cited by 34 publications

(47 citation statements)

References 39 publications

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“…NRP1 was overexpressed in various cancers including lung cancer, hepatocellular carcinoma, prostate cancer, and glioblastoma 27,28,29,30 .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-19b-3p suppresses gastric cancer development by negatively regulating Neuropilin-1

Wei¹,

Guo²,

Tang³

et al. 2020

Preprint

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Background Gastric cancer (GC) remains one of the most common digestive malignancies worldwide and ranked third causes of cancer-related death. Mounting evidence has revealed that miRNAs exert critical regulatory roles in GC development. Methods Immunohistochemistry (IHC) and western blot assay were performed to determine the protein expression levels of neuropilin-1 (NRP1) and mRNA levels were confirmed by quantitative RT-PCR (qRT-PCR) in GC tissues. Kaplan–Meier analysis was performed to evaluate the prognostic value of NRP1 in GC. Knockdown of NRP1 was conducted to analyse its function in vitro and vivo. Luciferase reporter assay, western blot and qRT-qPCR were employed to identify the miRNAs which directly targeted NRP1. Furthermore, Bioinformatics analysis and experimental verification were used to explore the potential molecular mechanism and signaling pathway. Results In the current study, we revealed that neuropilin-1 (NRP1) was highly expressed in GC tumor tissues and was associated with poor prognosis in GC patients. NRP1 knockdown inhibited GC cell growth, migration and invasion in vitro, while suppressed GC xenograft tumor development in vivo. Bioinformatics analysis predicted that miR-19b-3p down-regulated NRP1 expression by targeting its 3’-UTR. Functional assay demonstrated that miR-19b-3p inhibited GC cell growth, migration and invasion via negatively regulating NRP1. Overexpression NRP1 partially reversed the regulatory effect of miR-19b-3p. Moreover, we showed that miR-19b-3p/NRP1 axis regulated the epithelial-to-mesenchymal transition and focal adhesion in GC, which might contribute the GC development and progression. Conclusions Taken together, our findings suggest a regulatory network of miR-19b-3p/NRP1 in GC development. The miR-19b-3p/NRP1 axis might be further explored as a potential diagnostic and therapeutic target in GC.

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“…NRP1 was overexpressed in various cancers including lung cancer, hepatocellular carcinoma, prostate cancer, and glioblastoma 27,28,29,30 .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-19b-3p suppresses gastric cancer development by negatively regulating Neuropilin-1

Wei¹,

Guo²,

Tang³

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…Neuropilin 1 (NRP1) is a non-tyrosine kinase trans-membrane glycoprotein and is a co-receptor of semaphorin (SEMA)3A and vascular endothelial growth factor (VEGF) on the cell membrane. NRP1 plays an important role in angiogenesis, cell survival, migration and invasion, and could be a novel tumor marker ( 10 ). The expression of NRP1 is closely related to angiogenesis ( 11 ).…”

Section: Introductionmentioning

confidence: 99%

Effects of NRP1 on angiogenesis and vascular maturity in�endothelial cells are dependent on the expression of SEMA4D

et al. 2020

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Angiogenesis and vascular maturation play important roles in tumorigenesis and tumor development. The expression of neuropilin 1 (NRP1) is closely associated with angiogenesis in tumors; however, the molecular mechanisms of action in angiogenesis and tumor maturation, as well as the potential clinical value of NRP1 remain unclear. The importance of NRP1 expression in tumor progression was determined using The Cancer Genome Atlas (TCGA) database analysis. Gain- and loss-of-function experiments of NRP1 were performed in vascular endothelial cells (ECs) to investigate the functions in angiogenesis. CCK-8, flow cytometry, Transwell experiments and a series of in vitro experiments were used to detect cell functions. A combination of angiogenesis antibody arrays and RNA-Seq analyses were performed to reveal the proangiogenic mechanisms of action. The function of semaphorin 4D (SEMA4D) was also investigated separately. NRP1 mRNA levels were significantly increased in primary tumors compared with normal tissues based on TCGA data (P<0.01) and were associated with tumor development in patients. Gain- and loss-of-function experiments highlighted the function of NRP1 in promoting EC proliferation, motility and capillary-like tube formation and in reducing apoptosis. NRP1 overexpression led to significantly decreased EC markers (PECAM-1, angiogenin, PIGF and MMP-9) expression levels and reduced the vascular maturity. MAPK7, TPM1, RRBP1, PTPRK, HSP90A, PRKD2, PFKFB3, RGS4 and SPARC were revealed to play important roles in this process. SEMA4D was revealed to be a key protein associated with NRP1 in ECs. These data indicated that NRP1-promoted angiogenesis may be induced at the cost of reducing maturity of the ECs. NRP1 may also be a therapeutic target for antiangiogenic strategies and a candidate prognostic marker for tumors.

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“…NRP1-and NRP2-knockout mice have hypoplasia and deficiency in the neural system, emphasizing their roles in neural development [14] . NRP1 has been shown to be overexpressed in numerous human tumour tissues, including breast, lung, colorectal, and hepatocellular cancer [5,15] . Further, the expression of NRP1 is positively associated with prostatespecific antigen and Gleason score in prostatic cancer [16] , and overexpression may contribute to autocrine-paracrine interactions in pancreatic cancer [17] .…”

Section: Discussionmentioning

confidence: 99%

The NRP1 gene regulates proliferation, apoptosis, migration, and invasion in T24 and 5637 bladder cancer cells

Han

Dong

Hao

et al. 2020

Preprint

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Background Bladder urothelial carcinoma (BC) is a fatal invasive malignancy and the most common malignancy of the urinary system. In the current study, we investigate the function and mechanisms of Neuropilin-1 (NRP1), the co-receptor for vascular endothelial growth factor, in BC pathogenesis and progression. Methods The expression of NRP1 was assessed in several BC cell lines. Additionally, the biological function of NRP1 in proliferation, apoptosis, angiogenesis, migration, and invasion of BC were validated in vitro by silencing NRP1. Moreover, gene expression profiling chip analysis was conducted, and the related signalling pathways were confirmed by Western blot to reveal the potential molecular mechanisms by which NRP1 promotes the malignant progression of BC. Results Overexpression of NRP1 was observed in several human BC cell lines. NRP1 knockdown inhibited cell proliferation, promoted apoptosis, and decreased angiogenesis, migration, and invasion in T24 and 5637 human BC cells. Microarray analysis results indicated that the expression of NRP1 was correlated with the levels of cyclin dependent kinase (CDK) 4, baculoviral IAP repeat containing 3, Cyclin E 2, CDK2, and AP-1 transcription factor subunit in BC. We also demonstrated that the biological function of NRP1was associated with activation of the mitogen-activated protein kinase (MAPK) signalling pathway. Conclusions Our findings provide evidence that NRP1, as a potential tumour promoter, contributes to the metastasis and invasion of BC, which is associated with the activation of the MAPK pathway. Targeting NRP1 has the potential to become a new therapeutic strategy to benefit more patients with BC or other cancers.

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Neuropilin 1 (NRP1) is a novel tumor marker in hepatocellular carcinoma

Cited by 34 publications

References 39 publications

MicroRNA-19b-3p suppresses gastric cancer development by negatively regulating Neuropilin-1

MicroRNA-19b-3p suppresses gastric cancer development by negatively regulating Neuropilin-1

Effects of NRP1 on angiogenesis and vascular maturity in�endothelial cells are dependent on the expression of SEMA4D

The NRP1 gene regulates proliferation, apoptosis, migration, and invasion in T24 and 5637 bladder cancer cells

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