Background: Nasopharyngeal carcinoma (NPC) is a common malignant tumor of the head and neck region with poorly understood progression and prognosis. The present study aims at exploring whether the expression of β-catenin, TCF-4, and survivin affects clinicopathological features and prognostic significance in NPC.
Methods: We enrolled 164 patients with NPC and 70 patients with chronic nasopharyngitis (CNP) in this study. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC) were conducted to evaluate the expression of β-catenin, TCF-4, and survivin. Spearman's rank correlation analysis and Pearson correlation analysis were used to measure the correlation of β-catenin, TCF-4, and survivin. Risk factors for prognosis and survival conditions of NPC patients were analyzed by Cox proportional hazards model and Kaplan-Meier curves.
Results: The results obtained revealed that mRNA and protein expression of β-catenin, TCF-4, and survivin was higher in NPC tissues than in CNP tissues. Positive correlations amongst β-catenin, TCF-4, and survivin were identified by Spearman's rank correlation analysis and Pearson correlation analysis. There was a significant correlation in expression of β-catenin, TCF-4, and survivin with EBV DNA, EBV-VCA-IgA, EBV-EA-IgA, T stage, N stage, and clinicopathological stages. Lower overall survival (OS), distant metastasis-free survival (DMFS), local recurrence-free survival (LRFS), and disease-free survival (DFS) rates were detected in NPC patients with positive expression of β-catenin, TCF-4, and survivin, in contrast to those with negative expression. Cox proportional hazards model demonstrated that β-catenin, TCF-4, and survivin protein positive expression were independent risk factors for OS and DFS of NPC prognosis; there was an evident correlation between clinicopathological stages, TCF-4, and EBV-EA-IgA and OS, DMFS, LRFS, and DFS of NPC.
Conclusions: The aforementioned results indicate that β-catenin, TCF-4, and survivin proteins are highly expressed in NPC, which can be used as factors to predict the malignancy of NPC. In addition, positive expression of β-catenin, TCF-4, and survivin are potential risk factors that lead to an unfavorable prognosis of OS and DFS in NPC patients.
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http://dx.doi.org/10.1186/s12935-019-0764-7 | DOI Listing |
Life Sci
October 2024
Pharmaceutics and Industrial Pharmacy Department, Faculty of Pharmacy, Beni-Suef University, Beni-Suef, Egypt. Electronic address:
Discov Oncol
June 2024
Department of Gastrointestinal Surgery, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, People's Republic of China.
Background: By complexing poly (ADP-ribose) (PAR) in reaction to broke strand, PAR polymerase1 (PARP1) acts as the key enzyme participated in DNA repair. However, recent studies suggest that unrepaired DNA breaks results in persistent PARP1 activation, which leads to a progressively reduce in hexokinase1 (HK1) activity and cell death. PARP-1 is TCF-4/β-A novel co activator of gene transactivation induced by catenin may play a role in the development of colorectal cancer.
View Article and Find Full Text PDFBiochem Biophys Rep
July 2024
Department of Tropical Medicine, Yonsei University College of Medicine, Seoul, 03722, South Korea.
Proinflammatory cytokine plays a central role in host defense and acute inflammatory responses. Both positive and negative correlations of NF-κB and Wnt/β-catenin pathways have been reported depending on cell types in response to inflammatory stimuli for IL-6 cytokine production. Macrophages are vital to the regulation of immune responses and the development of inflammation, but the crosstalk between two pathways has not been elucidated so far in macrophages.
View Article and Find Full Text PDFMethods Mol Biol
February 2024
Centre de Recherche des Cordeliers, Sorbonne Université, Inserm, Université de Paris, Paris, France.
In recent years, important efforts have been made to understand how the expression of a specific gene repertoire correlates with chromatin accessibility, histone mark deposition, as well as with chromatin looping establishing connectivity with regulatory regions. The emergence of new techniques for genome-wide analyses and their progressive optimization to work on low amounts of material allows the scientific community to obtain an integrated view of transcriptional landscapes in physiology and disease. Here, we describe our own experience aiming at correlating the TCF-4/β-catenin cistrome during liver tumorigenesis with chromatin remodeling, histone mark modifications, and long-distance DNA looping.
View Article and Find Full Text PDFMol Ther
April 2024
Centre de Recherche des Cordeliers, Sorbonne Université, Inserm, Université Paris Cité, F-75006 Paris, France; Team « Oncogenic functions of beta-catenin signaling in the liver », Équipe labellisée par la Ligue Nationale contre le Cancer, F-75013 Paris, France; APHP, Institut du Cancer Paris CARPEM, F-75015 Paris, France. Electronic address:
The CTNNB1 gene, encoding β-catenin, is frequently mutated in hepatocellular carcinoma (HCC, ∼30%) and in hepatoblastoma (HB, >80%), in which DLK1/DIO3 locus induction is correlated with CTNNB1 mutations. Here, we aim to decipher how sustained β-catenin activation regulates DLK1/DIO3 locus expression and the role this locus plays in HB and HCC development in mouse models deleted for Apc (Apc) or Ctnnb1-exon 3 (β-catenin) and in human CTNNB1-mutated hepatic cancer cells. We identified an enhancer site bound by TCF-4/β-catenin complexes in an open conformation upon sustained β-catenin activation (DLK1-Wnt responsive element [WRE]) and increasing DLK1/DIO3 locus transcription in β-catenin-mutated human HB and mouse models.
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