ArticleHuman cell2024
Glycolysis Modulation by METTL7B Shapes Acute Lymphoblastic Leukemia Cell Proliferation and Chemotherapy Response.
Article in Human cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- METTL7B attenuates pathological cardiac hypertrophy via m6A-associated regulation of HK3.Molecular and cellular biochemistry · 2026Article
- The methyltransferase-like proteins as core regulators of nucleic acid modifications and post-translation modification of proteins in disease pathogenesis and therapeutic implications.Biomarker research · 2025Review
- HOXB4/METTL7B cascade mediates malignant phenotypes of hepatocellular carcinoma through TKT m6A modification.Biology direct · 2025Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Acute lymphoblastic leukemia (ALL) is a devastating hematological malignancy characterized by uncontrolled proliferation of immature lymphoid cells. While advances in treatment have improved patient outcomes, challenges remain in enhancing therapeutic efficacy and understanding underlying molecular mechanisms. Methyltransferase-like 7B (METTL7B), known for its methyltransferase activity, has been implicated in various solid tumors, yet its role in ALL remains unexplored. Here, we reveal that high METTL7B expression is correlated with poorer prognosis in ALL patients. Employing genetic manipulation strategies, we demonstrate that METTL7B depletion reduces ALL cell proliferation and enhances chemosensitivity. Mechanistically, we uncover METTL7B's involvement in modulating glycolysis, a crucial metabolic pathway supporting ALL cell growth. Furthermore, METTL7B's methyltransferase activity is identified as a determinant of its impact on glycolysis and proliferation. This study sheds light on METTL7B's multifaceted role in ALL, highlighting its potential as a therapeutic target and offering insights into the metabolic rewiring crucial for ALL progression.
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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 Socratic graph.