Synergistic effect of p53 on TSA-induced stanniocalcin 1 expression in human nasopharyngeal carcinoma cells, CNE2

Human stanniocalcin 1 (STC1) has recently been identified as a putative protein factor involved in cellular apoptosis. The use of histone deacetylase inhibitor (i.e. trichostatin A (TSA)) and doxorubicin (Dox) is one of the common treatment methods to induce apoptosis in human cancer cells. A study on TSA and Dox-mediated apoptosis may shed light on the regulation and function of STC1 in cancer treatment. In this study, TSA and Dox cotreatment in human nasopharyngeal carcinoma cells (CNE2) elicited synergistic effects on STC1 gene expression and cellular apoptosis. An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities. To elucidate the possible involvement of p53 in STC1 gene transcription, a vector expressing wild-type or dominant negative (DN) p53 was transiently transfected into the cells. Both STC1 promoter luciferase constructs and chromatin immunoprecipitation assays did not support the direct role of p53 in STC1 gene transactivation. However, the synergistic effects of p53 on the induction of NF-κB phosphorylation and the recruitment of acetylated histone H3 in STC1 promoter were observed in TSA-cotreated cells. The overexpression of exogenous STC1 sensitized apoptosis in Dox-treated cells. Taken together, this study provides data to show the cross talk of NF-κB, p53, and histone protein in the regulation of STC1 expression and function.

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Increased cyclin B1/CDC 2 kinase activity and phosphorylation of Bcl-2 associated with paclitaxel-induced apoptosis in human nasopharyngeal carcinoma cells

APOPTOSIS ◽

10.1007/bf01321020 ◽

1996 ◽

Vol 1 (2) ◽

pp. 141-146 ◽

Cited By ~ 4

Author(s):

C-H. Shu ◽

W. K. Yang ◽

T-S. Huang

Keyword(s):

Nasopharyngeal Carcinoma ◽

Kinase Activity ◽

Cyclin B1 ◽

Carcinoma Cells ◽

Human Nasopharyngeal Carcinoma ◽

Induced Apoptosis ◽

Cdc 2

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DNA sequences in human nasopharyngeal carcinoma cells that specify susceptibility to tumor promoter-induced neoplastic transformation

Carcinogenesis ◽

10.1093/carcin/8.1.121 ◽

1987 ◽

Vol 8 (1) ◽

pp. 121-127 ◽

Cited By ~ 10

Author(s):

Michael I. Lerman ◽

Ayako Sakai ◽

Yao Kai-Tai ◽

Nancy H. Colburn

Keyword(s):

Nasopharyngeal Carcinoma ◽

Dna Sequences ◽

Neoplastic Transformation ◽

Carcinoma Cells ◽

Tumor Promoter ◽

Human Nasopharyngeal Carcinoma

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Suppression of vascular endothelial growth factor via siRNA interference modulates the biological behavior of human nasopharyngeal carcinoma cells

Japanese Journal of Radiology ◽

10.1007/s11604-011-0603-9 ◽

2011 ◽

Vol 29 (9) ◽

pp. 615-622 ◽

Cited By ~ 6

Author(s):

Hai B. Zhou ◽

Yi F. Yin ◽

Yan Hu ◽

Xin Li ◽

Li Y. Zou ◽

...

Keyword(s):

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Nasopharyngeal Carcinoma ◽

Carcinoma Cells ◽

Biological Behavior ◽

Vascular Endothelial ◽

Human Nasopharyngeal Carcinoma ◽

Sirna Interference ◽

Endothelial Growth Factor

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miR-206 regulates a metabolic switch in nasopharyngeal carcinoma by suppressing HK2 expression

10.21203/rs.3.rs-43672/v1 ◽

2020 ◽

Author(s):

Chunying Luo ◽

Min Liu ◽

Jianwei Zhang ◽

Guoqiang Su ◽

Zhonghua Wei

Keyword(s):

Nasopharyngeal Carcinoma ◽

Warburg Effect ◽

Carcinoma Cells ◽

Luciferase Reporter ◽

Metabolic Shift ◽

Invasion And Metastasis ◽

Metabolic Switch ◽

And Function ◽

The Relationship

Abstract Background: Many studies have shown that microRNAs play key functions in nasopharyngeal carcinoma proliferation, invasion and metastasis. However, whether the dysregulated level of miRNAs contributes to the metabolic shift in nasopharyngeal carcinoma is not completely understood.Objectives: This study was conducted to explore the expression and function of miR-206 in nasopharyngeal carcinoma.Methods: miR-206 expression level was examined by real-time PCR. miR-206 inhibitor, mimics, and scrambled control were transiently transfected into nasopharyngeal carcinoma cells and their effects on colony formation, glucose uptake, and lactate secretion were observed in vitro. Moreover, the relationship between the levels of miR-206 and HK2 was examined by luciferase reporter and assay western blot.Results: In our study, we reported downregulation of miR-206 expression leads to metabolic change in nasopharyngeal carcinoma cells. miR-206 controls this function by enhancing HK2 expression. The enhancement of aerobic metabolism activity induced by miR-206 leads to the rapid proliferation of nasopharyngeal carcinoma cells.Conclusions: Our data demonstrated that miR-206 was involved in the regulation of Warburg effect in nasopharyngeal carcinoma by suppressing HK2 expression.

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