Association between the expression of HIF-1α and VEGF and prognostic implications in primary liver cancer

Guo, Liangliang; Zhu, Pei‐Wen; Jin, Xuanshun

doi:10.4238/gmr.15028107

Cited by 20 publications

(18 citation statements)

References 25 publications

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“…As an important multi-functional angiogenesis factor, VEGF exerts its function by specifically acting on receptors on the vascular endothelial cell surface, which cannot only promote mitosis and proliferation of vascular endothelial cells but also enhance capillary permeability (23). upregulated VEGF expression can be observed in all malignant tumors, and thus it plays a vital role in angiogenesis, infiltration and metastasis of tumors (24). To our surprise, we found that microRNA-26b significantly suppressed the NF-κB/MMP-9/VEGF pathway.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-26b inhibits the tumor growth of human liver cancer through the PI3K/Akt and NF-κB/MMP-9/VEGF pathways

Yan

Zhang

2018

Oncol Rep

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We investigated the role of microRNA-26b signaling in mediating the tumor growth of human liver cancer. MicroRNA-26b expression was observably downregulated in human liver cancer tissue. Forced upregulation of microRNA-26b had anticancer effects, inhibited cell proliferation, induced apoptosis and promoted Bax and caspase-3/-9 protein expression in a liver cancer cell line as determined by MTT assay, flow cytometry and western blot analysis. MicroRNA-26b significantly suppressed the PI3K/Akt and NF-κB/MMP-9/VEGF pathways. PI3K inhibitor significantly facilitated the effects of microRNA-26b regarding the suppression of the PI3K/Akt pathway, inhibition of cell proliferation, induction of apoptosis and increases in Bax and caspase-3/-9 protein expression in the liver cancer cell line. NF-κB inhibitor also significantly enhanced the effects of microRNA-26b regarding suppression of the NF-κB/MMP-9/VEGF pathway, inhibition of cell proliferation, induction of apoptosis, and promotion of Bax and caspase-3/-9 protein expression in the liver cancer cell line. The present study demonstrated that microRNA-26b inhibits the tumor growth of human liver cancer through the PI3K/Akt and NF-κB/MMP-9/VEGF pathways.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-26b inhibits the tumor growth of human liver cancer through the PI3K/Akt and NF-κB/MMP-9/VEGF pathways

Yan

Zhang

2018

Oncol Rep

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“…Angiogenesis has been recognized as the essential condition for cancer growth, while VEGF has been identified as its critical regulator. VEGF was overexpressed within liver tumor, and VEGF level showed significant relationship with the clinical classification as well as lymph node and lung metastases [30]. CEP55 may promote liver tumor cell growth and metastasis through the VEGF signaling pathway.…”

Section: Biomed Research Internationalmentioning

confidence: 95%

Upregulation of CEP55 Predicts Dismal Prognosis in Patients with Liver Cancer

Yang

Zhang

et al. 2020

BioMed Research International

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Purpose. This study was performed to investigate the association of CEP55 expression with liver cancer and explore potential underlying mechanisms. Materials and Methods. Data obtained from The Cancer Genome Atlas (TCGA) was used to investigate CEP55 expression, its prognostic value, the potential mechanisms of its upregulation, CEP55-related pathways, and its biological functions in liver cancer. Data from Gene Expression Omnibus (GEO) and International Cancer Genome Consortium (ICGC) was used to validate survival analysis. The correlation between CEP55 and tumor-infiltrating immune cells (TIICs) in liver cancer was determined by using Tumor Immune Estimation Resource (TIMER). Results. CEP55 was significantly overexpressed in the liver tumor sample compared to the adjacent normal liver sample. High CEP55 expression was significantly associated with histological grade, advanced stages, histological type, high T classification, and survival status. High CEP55 expression was significantly related to dismal prognosis compared with low CEP55 expression, which was validated by the GSE54236 dataset and ICGC database. Meanwhile, CEP55 was identified as the risk factor to independently predict overall survival (OS) for patients with liver cancer upon multivariate analysis. Enrichment analysis indicated that cell cycle, DNA replication, pathways in cancer, mTOR signaling pathway, and VEGF signaling pathway were significantly enriched in the high CEP55 expression group. In addition, the CEP55 expression was significantly related to the infiltration level of B cells, CD4+ T cells, CD8+ T cells, macrophages, neutrophils, and dendritic cells in hepatocellular carcinoma (HCC). CEP55 methylation level was negatively correlated to its mRNA expression. And patients with CEP55 hypermethylation and low expression can achieve a better prognosis than those with CEP55 hypomethylation and high expression. Conclusion. CEP55 may serve as a candidate treatment target for it is a determinant of prognosis and immune infiltration in liver cancer patients. DNA hypomethylation might contribute to the overexpression of CEP55 in liver cancer.

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“…Patients with hypoxic tumors, such as breast, endometrial, and liver, have a worse prognosis [18-20]. Moreover, hypoxia and HIF-1α overexpression are related to increased metastasis and resistance to conventional therapies, key factors that are responsible for cancer-related deaths [21, 22].…”

Section: Introductionmentioning

confidence: 99%

Glycobiology Modifications in Intratumoral Hypoxia: The Breathless Side of Glycans Interaction

Silva-filho¹,

Sena²,

Lima

et al. 2017

Cell Physiol Biochem

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Post-translational and co-translational enzymatic addition of glycans (glycosylation) to proteins, lipids, and other carbohydrates, is a powerful regulator of the molecular machinery involved in cell cycle, adhesion, invasion, and signal transduction, and is usually seen in both in vivo and in vitro cancer models. Glycosyltransferases can alter the glycosylation pattern of normal cells, subsequently leading to the establishment and progression of several diseases, including cancer. Furthermore, a growing amount of research has shown that different oxygen tensions, mainly hypoxia, leads to a markedly altered glycosylation, resulting in altered glycan-receptor interactions. Alteration of intracellular glucose metabolism, from aerobic cellular respiration to anaerobic glycolysis, inhibition of integrin 3α1β translocation to the plasma membrane, decreased 1,2-fucosylation of cell-surface glycans, and galectin overexpression are some consequences of the hypoxic tumor microenvironment. Additionally, increased expression of gangliosides carrying N-glycolyl sialic acid can also be significantly affected by hypoxia. For all these reasons, it is possible to realize that hypoxia strongly alters glycobiologic events within tumors, leading to changes in their behavior. This review aims to analyze the complexity and importance of glycoconjugates and their molecular interaction network in the hypoxic context of many solid tumors.

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Association between the expression of HIF-1α and VEGF and prognostic implications in primary liver cancer

Cited by 20 publications

References 25 publications

MicroRNA-26b inhibits the tumor growth of human liver cancer through the PI3K/Akt and NF-κB/MMP-9/VEGF pathways

MicroRNA-26b inhibits the tumor growth of human liver cancer through the PI3K/Akt and NF-κB/MMP-9/VEGF pathways

Upregulation of CEP55 Predicts Dismal Prognosis in Patients with Liver Cancer

Glycobiology Modifications in Intratumoral Hypoxia: The Breathless Side of Glycans Interaction

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