Background: Several isoforms of p53 have been reported, which may have varying functions and expressions. This study aimed to analyze the expression patterns of p53 isoforms in renal cell carcinoma (RCC) at the mRNA and protein levels and their associations with clinical and pathologic factors to explore the mechanism of p53 isoforms' activity in RCC.
Methods: The specimens of tumours (T) and clinically normal tissues (N) adjacent to them were collected from 41 patients with RCC. mRNA expression levels of p53 isoforms were detected using RT-PCR followed by nested PCR. Protein expression levels were detected using immunohistochemisty and Western blotting with the anti-p53 antibodies DO-1 and DO-12. The data were analyzed with clinicopathological features by chi(2) test or Fisher's exact test.
Results: p53 mRNA was expressed in all tumours and matched clinically normal tissue adjacent to the tumour. All six isoforms could be detected in tumour and normal tissues, with the exception of the Delta133p53beta isoform, which was not detected in the normal tissue. Of the six isoforms, p53beta mRNA was significantly overexpressed in tumour samples (P < 0.001), and correlated with tumour stage. Nested PCR results consistently indicated the presence of p53gamma (19T/22N), Delta133p53 (33T/26N), Delta133p53beta (2T/0N), and Delta133p53gamma (13T/9N). Immunohistochemical analysis showed that p53 was expressed only in tumour tissues and correlated with tumour stage and grade. The results of Western blotting analysis were consistent with these findings.
Conclusions: Although all six isoforms are present in RCC, their function in tumour development or progression might be different. Our findings suggest that p53beta might play an important role in the formation of RCC and it might be used as a new predictor and therapeutic target for RCC.
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Cell Death Dis
January 2025
Center for Precision Medicine Research, Marshfield Clinic Research Institute, Marshfield Clinic Health System, Marshfield, WI, USA.
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Univ Rouen Normandie, Inserm U1245, Normandie Univ, CHU Rouen, Department of Genetics, F-76000, Rouen, France
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Department of Biosciences, Biotechnologies, and Environment, University of Bari Aldo Moro, Italy. Electronic address:
Lysine-specific demethylase 1 (LSD1) is a key regulator in cancer epigenetic, and its activity is reliant on flavin adenine dinucleotide (FAD) as a cofactor. In this study, we investigated the correlation between LSD1 and FAD synthase isoform 2 (FADS2) protein levels in pancreatic ductal adenocarcinoma (PDAC) cell lines. We first assessed LSD1 protein and mRNA levels in mutant p53-expressing PANC-1 and MiaPaCa2 cells and p53-null AsPc-1 cells, compared to human pancreatic ductal epithelial (HPDE) controls.
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January 2025
Institute of Biophysical Chemistry and Center for Biomolecular Magnetic Resonance, Goethe University, 60438, Frankfurt, Germany.
The transcription factor p63 is expressed in many different isoforms as a result of differential promoter use and splicing. Some of these isoforms have very specific physiological functions in the development and maintenance of epithelial tissues and surveillance of genetic integrity in oocytes. The ASPP family of proteins is involved in modulating the transcriptional activity of the p53 protein family members, including p63.
View Article and Find Full Text PDFSci Rep
January 2025
Department of General Surgery, XiangYa Hospital Central South University, No. 87 XiangYa Road, Changsha, 410008, Hunan, China.
Papillary thyroid cancer (PTC) is often characterized by indolent behavior, small tumors with slow cell proliferation and a tendency to metastasize to cervical lymph node simultaneously, and the molecular mechanisms underlying that remain poorly understood. In this study, FN1 was the hottest gene of PTC and distinctive expression in PTC cells. FN1 deficiency severely inhibited the p53 signaling pathway, especially cyclin proteins, resulting in increased cell growth but hampered invasion.
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