ArticleBioengineered2021
Knockdown of lysine (K)-specific demethylase 2B KDM2B inhibits glycolysis and induces autophagy in lung squamous cell carcinoma cells by regulating the phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin pathway.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- KDM2B controls HIF levels and activity through its JmjC and CxxC domains.The Biochemical journal · 2026Article
- Review
- Histone demethylases in autophagy and inflammation.Cell communication and signaling : CCS · 2025Review
- Sevoflurane Confers Protection Against the Malignant Phenotypes of Lung Cancer Cells via the microRNA-153-3p/HIF1α/KDM2B Axis.Biochemical genetics · 2024Article
- MAZ-mediated up-regulation of BCKDK reprograms glucose metabolism and promotes growth by regulating glucose-6-phosphate dehydrogenase stability in triple-negative breast cancer.Cell death & disease · 2024Article
- Energy metabolism as the hub of advanced non-small cell lung cancer management: a comprehensive view in the framework of predictive, preventive, and personalized medicine.The EPMA journal · 2024Review
- Glutamine Supplementation as an Anticancer Strategy: A Potential Therapeutic Alternative to the Convention.Cancers · 2024Review
- PI3K/mTOR inhibitors promote G6PD autophagic degradation and exacerbate oxidative stress damage to radiosensitize small cell lung cancer.Cell death & disease · 2023Article
- KDM2B regulates inflammation and oxidative stress of sepsis via targeting NF-κB and AP-1 pathways.Immunity, inflammation and disease · 2023Article
- miR-199a: A Tumor Suppressor with Noncoding RNA Network and Therapeutic Candidate in Lung Cancer.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung squamous cell carcinoma (LUSC) is a subtype of non-small cell lung cancer with poor prognosis. This study aimed to explore the role of KDM2B in the development of LUSC. The results of this study demonstrated that KDM2B was upregulated in LUSC tissues and cell lines. Knockdown of KDM2B reduced cell viability and colony forming ability in SK-MES-1 and NCI-H520 cells. KDM2B inhibition reduced glucose consumption, lactate production, ATP level, and also downregulated the expression of LDHA and GLUT1. KDM2B knockdown decreased the protein expression of LC3-I and p62, and increased LC3-II and Beclin-1. Furthermore, KDM2B silencing inhibited the phosphorylation of AKT, mTOR and P70S6K. KDM2B knockdown led to reduced tumor size in mouse model. In conclusion, KDM2B is upregulated in LUSC tissues and cell lines. KDM2B silencing inhibits glycolysis and promotes autophagy through inactivation of the PI3K/Akt/mTOR signaling pathway.
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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.