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Leo I. Gordon, MD, FACP
Leo I. Gordon, MD, FACP
Posted: Tuesday, March 15, 2022
Transcription factor 3 (TCF3) combined with histone deacetylase 3 (HDAC3) has been found to downregulate the expression of microRNA-101, supporting the production of Burkitt lymphoma cells and preventing their apoptosis, according to a study published in the journal Bioengineered. “This study suggests that TCF3 can be a biological marker of Burkitt lymphoma and may be a potential therapeutic target for this disease,” noted Yufu Li, MD, of the Affiliated Cancer Hospital of Zhengzhou University, China, and colleagues.
Tumor tissue samples were obtained from patients with Burkitt lymphoma as well as lymph node tissue samples from patients with reactive lymph node hyperplasia. Namalwa, Raji, and Daudi B-cell lines were also used in the study. Quantitative reverse transcriptase–polymerase chain reaction was performed on all samples to determine TCF3 expression, HDAC3, and microRNA-101. Additionally, researchers looked at the interaction between TCF3 and HDAC3 using co-immunoprecipitation, as well as chromatin immunoprecipitation to identify the development of TCF3 and HDAC3 in microRNA-101.
Study results suggest that TCF3 may play a role in the pathogenesis of Burkitt lymphoma. The researchers found that TCF3 can bind to HDAC3 and is enhanced in the microRNA-101 promoter region. Lastly, the targeted reduction of TCF3 was found to produce the same results as the overexpression of microRNA-101. This resulted in the impediment of Burkitt lymphoma cell proliferation, decreased cell viability, increased cell apoptosis, and inhibition of the expression of Akt/mTOR pathway–related proteins.
Further studies are needed to explore potential target genes that may be regulated by microRNA-101 in Burkitt lymphoma and how they relate to the clinicopathologic elements of the disease.
Disclosure: The study authors reported no conflicts of interest.
