State of the art paper Function and expression of prolyl hydroxylase 3 in cancers

Liu, Qiu-Long; Liang, Qiong; Li, Zhouyu; Zhou, Yuan; Ou, Wen‐Ting; Huang, Zhigang

doi:10.5114/aoms.2013.36987

Cited by 5 publications

(5 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Correlation analysis of PHD3 expression with regards to the clinicopathological features of gastric cancer revealed that increased PHD3 expression was correlated with a high degree of differentiation of cancer cells, early TNM stage and decreased lymph node metastasis. These results are consistent with previous studies (20,27) and suggest that PHD3, or a putative protein target downstream of PHD3, may participate in tumor progression. Su et al (25) reported that PHD3 was upregulated in well-differentiated specimens of pancreatic cancer, whereas undifferentiated tumors exhibited reduced PHD3 expression.…”

Section: Discussionsupporting

confidence: 93%

“…Chen et al (19) demonstrated that PHD3 protected the intestinal epithelial barrier from ulcerative injury, which is one of the causes leading to the development of gastric cancer. However, although the actions of PHD3 in the suppression of angiogenesis, growth and differentiation of tumor cells have previously been reported (20), the detailed molecular mechanisms implicating PHD3 in gastric cancer have yet to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

PHD3 affects gastric cancer progression by negatively regulating HIF1A

Xia

Jiang

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

Prolyl hydroxylase 3 (PHD3) is widely accepted as a tumor suppressor; however, the expression of PHD3 in various cancer types remains controversial. The present study aimed to investigate the association between PHD3 expression and the clinicopathological features of gastric cancer using reverse transcription‑quantitative polymerase chain reaction and immunohistochemistry. The effects of PHD3 in gastric cancer cell lines were assessed using western blot analysis and transwell migration assays. The present results revealed that PHD3 expression was increased in adjacent non‑cancerous tissue compared with in gastric cancer tissue, and PHD3 overexpression was correlated with the presence of well‑differentiated cancer cells, early cancer stage classification and the absence of lymph node metastasis. In vitro experiments demonstrated that PHD3 may act as a negative regulator of hypoxia‑inducible factor‑1α and vascular endothelial growth factor, both of which participate in tumor angiogenesis. In conclusion, the present results suggested that PHD3 may act as a tumor suppressor in gastric cancer. Therefore, the targeted regulation of PHD3 may have potential as a novel therapeutic approach for the treatment of patients with gastric cancer.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

PHD3 affects gastric cancer progression by negatively regulating HIF1A

Xia

Jiang

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

show abstract

“…The present study aimed to explore the association between PHD3 and HIF2α expression in HCC (under hypoxic conditions). Several studies have demonstrated that PHD3 serves a novel role in the progression and prognosis of cancer (15-24); PHD3 is also able to induce apoptosis and inhibit proliferation in cancer cells (22)(23)(24)(25)(26)(27)(28)(29). To the best of our knowledge, the present study is the first to report that PHD3 overexpression induces apoptosis and inhibits growth and proliferation in HCC cells.…”

Section: Introductionmentioning

confidence: 59%

Association of PHD3 and HIF2α gene expression with clinicopathological characteristics in human hepatocellular carcinoma

et al. 2017

View full text Add to dashboard Cite

Abstract. Egl-9 family hypoxia-inducible factor (HIF)3/prolyl hydroxylase 3 (EGLN3/PHD3) serves a role in the progression and prognosis of cancer. PHD3 is able to induce apoptosis in HepG2 cells. In the present study, the protein levels of PHD3 and HIF2α were analyzed by western blot analysis and immunohistochemistry in 84 paired hepatocellular carcinoma (HCC) tissues and adjacent non-tumor liver tissues. The mRNA levels of PHD3 and HIF2α were analyzed by reverse transcription-quantitative polymerase chain reaction. PHD3 was overexpressed in HCC tissues compared with adjacent liver tissues (mRNA expression: P<0.001; protein expression: P=0.003; immunohistochemistry positive rate: P=0.001). The high level of expression of PHD3 in HCC tissues was associated with good differentiation (mRNA expression: P=0.002; protein expression: P<0.001) and small tumor size (mRNA expression: P<0.001; protein expression: P=0.002). In addition, HIF2α expression was lower in HCC tissues compared with adjacent liver tissues (mRNA expression: P<0.001; protein expression: P=0.002; immunohistochemistry positive rate: P= 0.002). No statistically significant associations were identified between HIF2α expression and clinicopathological characteristics. Pearson's and Spearman's correlation coefficients revealed no correlation between HIF2α and PHD3 expression in HCC. In conclusion, PHD3 expression acts as a favorable prognostic marker for patients with HCC. There is no correlation between PHD3 and HIF2α expression in HCC.

show abstract

“…Thus, PHD3 appears to have oncosuppressive properties in many different tumors, with low levels of the enzyme correlating with poor outcome. This is the case of pancreatic, colorectal, and breast cancers [ 53 ], plasma cell neoplasia [ 54 ], pheochromocytoma [ 55 ] and glioblastoma [ 56 ], where PHD3 regulates neuronal apoptosis. PDH3, together with its downstream effectors, defines a pathway that is responsible for the elimination of excess neuroblasts during normal embryological development when growth factors, such as NGF, become limiting.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical analysis of PDK1, PHD3 and HIF-1α expression defines the hypoxic status of neuroblastoma tumors

Ognibene¹,

Cangelosi²,

Morini³

et al. 2017

PLoS ONE

View full text Add to dashboard Cite

Neuroblastoma (NB) is the most common solid tumor during infancy and the first cause of death among the preschool age diseases. The availability of several NB genomic profiles improves the prognostic ability, but the outcome prediction for this pathology remains imperfect. We previously produced a novel prognostic gene signature based on the response of NB cells to hypoxia, a condition of tumor microenvironment strictly connected with cancer aggressiveness. Here we attempted to further define the expression of hypoxia-modulated specific genes, looking at their protein level in NB specimens, considering in particular the hypoxia inducible factor-1α (HIF-1α), the mitochondrial pyruvate dehydrogenase kinase 1 (PDK1), and the HIF-prolyl hydroxylase domain 3 (PHD3). The evaluation of expression was performed by Western blot and immunocytochemistry on NB cell lines and by immunohistochemistry on tumor specimens. Stimulation of both HIF-1α and PDK1 and inhibition of PHD3 expression were observed in NB cell lines cultured under prolonged hypoxic conditions as well as in most of the tumors with poor outcome. Our results indicate that the immunohistochemistry analysis of the protein expression of PDK1, PHD3, and HIF-1α defines the hypoxic status of NB tumors and can be used as a simple and relevant tool to stratify high-risk patients.

show abstract

State of the art paper Function and expression of prolyl hydroxylase 3 in cancers

Cited by 5 publications

References 44 publications

PHD3 affects gastric cancer progression by negatively regulating HIF1A

PHD3 affects gastric cancer progression by negatively regulating HIF1A

Association of PHD3 and HIF2α gene expression with clinicopathological characteristics in human hepatocellular carcinoma

Immunohistochemical analysis of PDK1, PHD3 and HIF-1α expression defines the hypoxic status of neuroblastoma tumors

Contact Info

Product

Resources

About