ArticleMedical oncology (Northwood, London, England)2023
JMJD5 inhibits lung cancer progression by regulating glucose metabolism through the p53/TIGAR pathway.
Article in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Fundamentals and emerging frontiers in p53-targeted drug development.Biochemistry and biophysics reports · 2026Review
- JMJD5: a multifunctional regulator in development, homeostasis, and cancer.Frontiers in cell and developmental biology · 2026Review
- Review
- TIGAR inhibits glucose-metabolism and cisplatin-chemosensitivity in human lung cancer cells.Discover oncology · 2025Article
- Immunonutrition, Metabolism, and Programmed Cell Death in Lung Cancer: Translating Bench to Bedside.Biology · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Metabolic reprogramming is considered one of the main driving forces for tumor progression, providing energy and substrates of biosynthesis to support rapid neoplastic proliferation. Particularly, the tumor suppressor protein p53 was shown to revert the Warburg effect and play complex roles in regulating glucose metabolism. Jumonji C domain-containing protein 5 (JMJD5) has previously been reported as a negative regulator of p53. However, the role of JMJD5 in p53-mediated metabolic reprogramming remains elusive. Here, we discovered that knockdown of JMJD5 significantly enhances TIGAR expression in p53 wild-type non-small cell lung cancer (NSCLC) cells, which could further suppress glycolysis and promote the pentose phosphate pathway. Besides, JMJD5 knockdown promotes the NSCLC cell proliferation in vitro and xenograft tumor growth in vivo, while silencing TIGAR can abolish this effect. Low JMJD5 expression levels are associated with elevated TIGAR levels and correlates with poor prognosis in lung cancer patients. Taken together, our findings suggest that JMJD5 is a key regulator of tumor glucose metabolism by targeting the p53/TIGAR metabolic pathway.
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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.