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MYO18B has been proposed to contribute to the progression of hepatocellular carcinoma (HCC). However, the signals that govern MYO18B transcription are not known. Here we show that, a network of C19MC miRNA-520G, IFN-γ, CEBPB and p53 transcriptional-defects promote MYO18B mRNA expression in HCCs. IFN-γ by itself suppresses MYO18B transcription, but promotes it when miRNA-520G is stably overexpressed. Similarly, CEBPB-liver-enriched activator protein (LAP) isoform overexpression suppresses MYO18B transcription but promotes transcription when the cells are treated with IFN-γ. Furthermore, miR-520G together with mutant-p53 promotes MYO18B transcription. Conversely, bFGF suppresses MYO18B mRNA irrespective of CEBPB, miR-520G overexpression or IFN-γ treatment. Finally high MYO18B expression reflects poor prognosis while high MYL5 or MYO1B expression reflects better survival of HCC patients. Thus, we identified a network of positive and negative regulators of MYO18B mRNA expression which reflects the survival of HCC patients.
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http://dx.doi.org/10.1038/s41598-020-69179-5 | DOI Listing |
Clin Epigenetics
April 2025
Henan Provincial Key Laboratory of Genetic Diseases and Functional Genomics and Medical, Genetics Institute of Henan Province, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, China.
Objective: Dilated cardiomyopathy (DCM)-associated heart failure (HF) presents a significant clinical challenge, underlying epigenetic mechanisms remaining poorly understood. This study aims to investigate the interplay between DNA methylation and gene expression in the hearts of patients with DCM-associated HF (DCM-HF).
Methods: Atrial tissues were collected from five healthy donors and five heart transplant recipients suffering from heart failure due to DCM.
Sci Rep
July 2020
Sarcoma Department, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL, 33612, USA.
MYO18B has been proposed to contribute to the progression of hepatocellular carcinoma (HCC). However, the signals that govern MYO18B transcription are not known. Here we show that, a network of C19MC miRNA-520G, IFN-γ, CEBPB and p53 transcriptional-defects promote MYO18B mRNA expression in HCCs.
View Article and Find Full Text PDFMol Med Rep
December 2019
Department of Rheumatology, Gansu Provincial Hospital, Lanzhou, Gansu 730000, P.R. China.
MicroRNAs serve an important role in the development of several diseases. Numerous genes regulate the skeletal muscle differentiation of C2C12 myoblasts. The role of miR‑760 in rheumatoid arthritis (RA) has not been reported, to the best of our knowledge.
View Article and Find Full Text PDFJ Neuromuscul Dis
September 2015
Department of Translational Medecine, IGBMC, Illkirch, France.
Background: Nemaline myopathies (NM) are rare and severe muscle diseases characterized by the presence of nemaline bodies (rods) in muscle fibers. Although ten genes have been implicated in the etiology of NM, an important number of patients remain without a molecular diagnosis.
Objective: Here we describe the clinical and histopathological features of a sporadic case presenting with severe NM and cardiomyopathy.
Mar Genomics
December 2014
Faculty of Biosciences and Aquaculture, University of Nordland, 8049 Bodø, Norway. Electronic address:
The circadian rhythm is a fundamental adaptive mechanism to the daily environmental changes experienced by many organisms, including fish. Myosins constitute a large family of contractile proteins that are essential functional components of skeletal muscle. They are known to display thermal plasticity but the influence of light on myosin expression remains to be investigated in fish.
View Article and Find Full Text PDF