Effect of hypoxia-inducible factor-1α on transcription of survivin in non-small cell lung cancer

Chen, Yuqing; Zhao, Chengling; Li, Wei

doi:10.1186/1756-9966-28-29

Cited by 64 publications

(62 citation statements)

References 25 publications

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“…In parallel with the induction of Notch-1 expression, survivin level is also strongly upregulated in A549 cells by hypoxia compared with normoxia, as described in our previous study. 25 Similarly, current reports highlighted that the overexpression of Notch-1 is accompanied by increased survivin level and in contrast, the inhibition of Notch-1 signaling by γ-secretase inhibitor abrogates oxaliplatin-induced survivin expression in colon cancer cells. 26 In addition, activation of Notch-1 signaling protects lung survivin expression, does the activation of Notch-1 pathway influence the production of survivin protein?…”

mentioning

confidence: 89%

Notch-1 signaling facilitates survivin expression in human non-small cell lung cancer cells

Chen

Li²,

Liu³

et al. 2011

Cancer Biology & Therapy

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confidence: 89%

Notch-1 signaling facilitates survivin expression in human non-small cell lung cancer cells

Chen

Li²,

Liu³

et al. 2011

Cancer Biology & Therapy

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“…[7][8][9] Consistent hypoxia could lead to resistance to apoptosis as well as treatments, but the molecular mechanisms are not fully understood. Some angiogenesis-related genes such as vascular growth factors (VEGF) and urokinasetype plasminogen activator receptor (uPAR) 10,11 as well as a few apoptosis regulators such as the anti-apoptotic Mcl-1, Bcl-xL and BIRC5/survivin [12][13][14] have been identified as target genes of HIF-1α. Aurora A (STK15) is an important member of Aurora kinase family, which is a novel family of serine/threonine kinases promoting mitotic spindle assembly by regulating centrosome duplication and separation.…”

Section: Introductionmentioning

confidence: 99%

The role of Aurora A in hypoxia-inducible factor 1α-promoting malignant phenotypes of hepatocelluar carcinoma

et al. 2013

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overexpression of both hypoxia-inducible factor 1α (HIF-1α) and aurora a has been found in hepatocelluar carcinoma (HCC). However, whether HIF-1α and aurora a synergistically promote malignant phenotypes of HCC cells is unknown. the purpose of this study was to investigate the roles and functional correlation of HIF-1α and aurora a in HCC progression. Immunohistochemistry was performed to detect HIF-1α and aurora a protein expression in 55 primary HCC and corresponding non-tumor tissues and their clinical significance. Gene knockout technology using short hairpin rNa (shrNa) was used to knockdown expression of HIF-1α or aurora a and analyze their effects on malignant phenotypes of HCC cells. the transcriptional regulation of aurora a by HIF-1α and the possible downstream molecular signaling pathways were also determined. results showed that hypoxia could induce the increased expression of HIF-1α and aurora a in HCC cells. also, shrNa-mediated HIF-1α downregulation could lead to the decreased aurora a expression and inhibition of growth or invasion in HCC cells. Moreover, HIF-1α could transcriptionally regulate aurora a expression by binding to hypoxia-responsive elements in the aurora a promoter and recruiting the coactivator-p300/ CBP. additionally, shrNa-mediated aurora a knockdown could mimic the effects of HIF-1α downregulation on phenotypes of HCC cells, and overexpression of aurora a could partially rescue the phenotypical changes of HCC cells induced by HIF-1α downregulation. Further research indicated that activation of akt and p38-MaPK signaling pathways mediated the downstream effects of HIF-1α and aurora a in HCC cells under hypoxic condition. taken together, our findings indicated that aurora a might be a key regulator of HIF-1α-promoting malignant phenotypes of HCC by activation of akt and p38-MaPK signaling pathways.

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“…This overexpression was also found to be correlated with poor patient prognosis in medulloblastoma and breast cancer (14)(15)(16)(17). HiF1-α and Survivin were found to be overexpressed in non-small-cell lung cancer, and their expression levels were demonstrated to be correlated (18). in this study, HiF1-α and Survivin were highly expressed in crc tissue.…”

Section: Discussionmentioning

confidence: 56%

Effect of hypoxia-inducible factor 1-α on Survivin in colorectal cancer

Fu²,

Wang³

2010

Mol Med Rep

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Abstract. colorectal cancer is a one of the most common malignancies. Hypoxia-inducible factor 1-α (HiF1-α) and Survivin play important roles in tumor development; however, the literature currently contains few reports on the relationship between them in colorectal cancer. in this study, we investigated the effect of HiF1-α on Survivin in colorectal cancer. immunohistochemical staining was used to detect the expression of HiF1-α and Survivin in colorectal cancer tissue from 32 patients. colon adenocarcinoma SW480 cells were cultured under normoxia and hypoxic conditions, and the expression of HiF1-α and Survivin was detected by rT-Pcr and Western blotting. We also silenced HiF1-α in order to detect the expression of Survivin and cell apoptosis. in an in vivo xenograft tumor model, the effect of HiF1-α on cancer development and Survivin was evaluated by the measurment of tumor volume and immunohistochemical analysis. analysis revealed that HiF1-α (75%) and Survivin (68.75%) were both overexpressed in colorectal cancer, and that their expression was correlated. They were also expressed in SW480 cells under conditions of normoxia, and exhibited a significant increase in expression under hypoxic conditions. The inhibition of HiF1-α by rna interference decreased the expression of Survivin and led to the apoptosis of the SW480 cell line. in the in vivo xenograft tumor model, the expression of HiF1-α and Survivin was decreased in the siHiF1-α group, and the tumor volume (586.67±41.63 mm 3 ) was much smaller than that in the negative interference (1374.67±85.87 mm 3 ) and salinetreated (1382.80±28.42 mm 3 ) groups. our results indicate that HiF1-α is an important regulator of Survivin expression and has great potential capacity for cancer therapeutics.

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Effect of hypoxia-inducible factor-1α on transcription of survivin in non-small cell lung cancer

Cited by 64 publications

References 25 publications

Notch-1 signaling facilitates survivin expression in human non-small cell lung cancer cells

Notch-1 signaling facilitates survivin expression in human non-small cell lung cancer cells

The role of Aurora A in hypoxia-inducible factor 1α-promoting malignant phenotypes of hepatocelluar carcinoma

Effect of hypoxia-inducible factor 1-α on Survivin in colorectal cancer

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