ArticleHematological oncology2025
Deubiquitinase TRIM44 Promotes Autophagy-Mediated Chemoresistance in Diffuse Large B Cell Lymphoma.
Article in Hematological oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- TRIM28 facilitates diffuse large B-cell lymphoma progression by inducing glycolytic reprogramming through the E2F1/PKM2 axis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- PRMT7-mediated arginine methylation of FOXK activates Wnt/β-catenin signalling to drive doxorubicin resistance in diffuse large B-cell lymphoma.Clinical and translational medicine · 2026Article
- Exploring CD79b, LC3, and TERT expression in NON-GCB DLBCL: markers associated with Rituximab-Cyclophosphamide-Doxorubicin-Vincristin-Prednisone treatment response.Blood research · 2026Article
- Crosstalk Between Allergic Inflammation and Autophagy.International journal of molecular sciences · 2025Review
- Deubiquitinase TRIM44 Promotes Autophagy-Mediated Chemoresistance in Diffuse Large B Cell Lymphoma.Hematological oncology · 2025Article
- The ubiquitination-autophagy axis in cancer therapy resistance: mechanistic insights and therapeutic opportunities.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Diffuse large B cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma. Tripartite motif containing 44 (TRIM44) belonging to the TRIM family, is involved in tumor development and is highly expressed in a variety of tumors. However, the role of TRIM44 in DLBCL remains undefined. Gain and loss-of-function studies were performed on lymphoblast cell lines DB and SU-DHL-4 to investigate its function. TRIM44 overexpression significantly promoted cell proliferation and viability, whereas its silencing inhibited proliferation and induced apoptosis. TRIM44 overexpression upregulated the LC3II/LC3-I ratio and Beclin1 expression, as well as increased autophagosomes formation, suggesting autophagy activation. Notably, TRIM44 conferred chemoresistance to doxorubicin in DB cells by increasing autophagic activity. In vivo study on mice revealed that TRIM44 overexpression increased Ki67 and PCNA expression, suggesting an increased tumor growth. Our previous work revealed that miR-665 is a tumor suppressor in DLBCL. The results of miRNA pull-down and luciferase reporter assay indicated that TRIM44 was a direct target of miR-665. In conclusion, TRIM44 promoted DLBCL progression by increasing autophagy-mediated chemoresistance, revealing the involvement of miR-665/TRIM44 axis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.