ArticleMolecular biotechnology2023
Long Non-coding RNA H19 Recruits NFYB to Activate MBTD1 and Regulate Doxorubicin Resistance in Lymphoma Cells.
Article in Molecular biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- NFYB-lncRNA axis resets the tumor microenvironment to promote HCC aggressive progression by a positive feedback loop.Acta pharmaceutica Sinica. B · 2026Article
- Diabetic Cardiomyopathy: Role of Cell Death, Exosomes, Fibrosis and Epicardial Adipose Tissue.International journal of molecular sciences · 2024Review
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Doxorubicin (DOX) is a first-line chemo drug for lymphoma treatment. DOX resistance remains a major obstacle leading to treatment failure. This study explores the interactions of the long non-coding RNA H19 (H19)/nuclear transcription factor Y subunit beta (NFYB)/mbt domain containing 1 (MBTD1) axis in DOX resistance in lymphoma cells. Bioinformatics prediction indicated a correlation between MBTD1 and advanced lymphoma stage. Elevated MBTD1 expression was detected in lymphoma cells compared to normal lymphocytes, especially in DOX-resistant lymphoma cells (OCI-Ly8/DOX and SU-DHL-2/DOX). MBTD1 silencing weakened DOX resistance in the drug-resistant cells. Bioinformatics analysis further indicated a candidate H19/NFYB/MBTD1 axis in lymphoma. Luciferase and ChIP-qPCR assays validated that NFYB bound to MBTD1 promoter to activate the MBTD1 transcription. H19 recruited NFYB to increase MBTD1 expression without altering NFYB levels. H19 silencing suppressed growth of the DOX-resistant cells in vitro and in vivo. Either NFYB or MBTD1 activation restored the DOX resistance and malignant growth of the cells. In summary, this paper demonstrates that H19 activates MBTD1 transcription in a NFYB-dependent manner to promote DOX resistance in lymphoma cells.
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Registered trials
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