Nogo‐B promotes tumor angiogenesis and provides a potential therapeutic target in hepatocellular carcinoma

Cai, Hao; Saiyin, Hexige; Liu, Xing; Han, Dingding; Ji, Guangchen; Qin, Bo; Zuo, Jie; Shen, Suqin; Yu, Wenbo; Wu, Jiaxue; Wu, Yanhua; Liu, Yu

doi:10.1002/1878-0261.12358

Cited by 9 publications

(12 citation statements)

References 43 publications

(54 reference statements)

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“…More recently it has been reported that the expression level of Nogo-B is upregulated in hepatocellular carcinoma and Nogo-B deficiency suppressed the tumor growth and metastasis [221]. The expression level of Nogo-B correlated with tumor vessel density in hepatocellular carcinoma and anti-Nogo-B antibody inhibited tumor growth in vivo via suppressing tumor angiogenesis [222].…”

Section: Other Proangiogenic Factors Contribute To Tumor Angiogenesismentioning

confidence: 98%

Tumor angiogenesis: causes, consequences, challenges and opportunities

Lugano

Ramachandran

Dimberg

2019

Cell. Mol. Life Sci.

1,024

834

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Tumor vascularization occurs through several distinct biological processes, which not only vary between tumor type and anatomic location, but also occur simultaneously within the same cancer tissue. These processes are orchestrated by a range of secreted factors and signaling pathways and can involve participation of non-endothelial cells, such as progenitors or cancer stem cells. Anti-angiogenic therapies using either antibodies or tyrosine kinase inhibitors have been approved to treat several types of cancer. However, the benefit of treatment has so far been modest, some patients not responding at all and others acquiring resistance. It is becoming increasingly clear that blocking tumors from accessing the circulation is not an easy task to accomplish. Tumor vessel functionality and gene expression often differ vastly when comparing different cancer subtypes, and vessel phenotype can be markedly heterogeneous within a single tumor. Here, we summarize the current understanding of cellular and molecular mechanisms involved in tumor angiogenesis and discuss challenges and opportunities associated with vascular targeting.

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Section: Other Proangiogenic Factors Contribute To Tumor Angiogenesismentioning

confidence: 98%

Tumor angiogenesis: causes, consequences, challenges and opportunities

Lugano

Ramachandran

Dimberg

2019

Cell. Mol. Life Sci.

1,024

834

View full text Add to dashboard Cite

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“…Our previous study indicated that Nogo‐B expression is significantly elevated in HCC and drastically promotes tumor angiogenesis 7 . Given hypoxia plays a critical role in the induction of angiogenic factors, Nogo‐B might also be induced by the hypoxic environment in tumor tissue.…”

Section: Resultsmentioning

confidence: 99%

“…However, the role of NgBR in tumor development is still in debate 50‐52 . Our previous study reported a novel Nogo‐B/integrin pathway that may promote tumor angiogenesis in multiple cancers, especially HCC 7 . Expression levels of Nogo‐B are significantly upregulated in HCC.…”

Section: Discussionmentioning

confidence: 99%

“…Our previous studies have shown that the expression level of Nogo‐B was significantly upregulated in HCC 6 . Increased Nogo‐B promoted tumor growth and angiogenesis 6,7 . However, the regulatory mechanism of Nogo‐B expression in HCC still remains unclear.…”

Section: Introductionmentioning

confidence: 99%

“…and angiogenesis. 6,7 However, the regulatory mechanism of Nogo-B expression in HCC still remains unclear.…”

mentioning

confidence: 99%

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Upregulation of Nogo‐B by hypoxia inducible factor‐1 and activator protein‐1 in hepatocellular carcinoma

et al. 2021

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Nogo‐B is an important regulator of tumor angiogenesis. Expression of Nogo‐B is remarkably upregulated in multiple tumor types, especially hepatocellular carcinoma (HCC). Here, we show the transcriptional regulation mechanisms of Nogo‐B in liver cancer. In response to hypoxia, expression of Nogo‐B significantly increased in HCC tissues and cells. The distal hypoxia‐responsive element in the promoter was essential for transcriptional activation of Nogo‐B under hypoxic conditions, which is the specific site for hypoxia inducible factor‐1α (HIF‐1α) binding. In addition, Nogo‐B expression was associated with c‐Fos expression in HCC tissues. Nogo‐B expression was induced by c‐Fos, yet inhibited by a dominant negative mutant A‐Fos. Deletion and mutation analysis of the predicted activator protein‐1 binding sites revealed that functional element mediated the induction of Nogo‐B promoter activity, which was confirmed by ChIP. These results indicate that HIF‐1α and c‐Fos induce the expression of Nogo‐B depending on tumor microenvironments, such as hypoxia and low levels of nutrients, and play a role in upregulation of Nogo‐B in tumor angiogenesis.

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Role of cellular, molecular and tumor microenvironment in hepatocellular carcinoma: Possible targets and future directions in the regorafenib era

Juengpanich

Topatana

et al. 2020

Intl Journal of Cancer

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Hepatocellular carcinoma (HCC) remains as one of the major causes of cancer‐related mortality, despite the recent development of new therapeutic options. Regorafenib, an oral multikinase inhibitor, is the first systemic therapy that has a survival benefit for patients with advanced HCC that have a poor response to sorafenib. Even though regorafenib has been approved by the FDA, the clinical trial for regorafenib treatment does not show significant improvement in overall survival. The impaired efficacy of regorafenib caused by various resistance mechanisms, including epithelial–mesenchymal transitions, inflammation, angiogenesis, hypoxia, oxidative stress, fibrosis and autophagy, still needs to be resolved. In this review, we provide insight on regorafenib microenvironmental, molecular and cellular mechanisms and interactions in HCC treatment. The aim of this review is to help physicians select patients that would obtain the maximal benefits from regorafenib in HCC therapy.

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Nogo‐B promotes tumor angiogenesis and provides a potential therapeutic target in hepatocellular carcinoma

Cited by 9 publications

References 43 publications

Tumor angiogenesis: causes, consequences, challenges and opportunities

Tumor angiogenesis: causes, consequences, challenges and opportunities

Upregulation of Nogo‐B by hypoxia inducible factor‐1 and activator protein‐1 in hepatocellular carcinoma

Role of cellular, molecular and tumor microenvironment in hepatocellular carcinoma: Possible targets and future directions in the regorafenib era

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