ArticleAmerican journal of cancer research2015
KDM5B is overexpressed in gastric cancer and is required for gastric cancer cell proliferation and metastasis.
Article in American journal of cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
43 citing papers in PubMed, 64 citations in OpenAlex.
- Roles of KDM5 demethylases in therapeutic resistance of cancers.Epigenetics & chromatin · 2025Review
- The WWP1-JARID1B axis sustains acute myeloid leukemia chemoresistance.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Co-targeting SKP2 and KDM5B inhibits prostate cancer progression by abrogating AKT signaling with induction of senescence and apoptosis.The Prostate · 2024Article
- KDM5B promotes SMAD4 loss-driven drug resistance through activating DLG1/YAP to induce lipid accumulation in pancreatic ductal adenocarcinoma.Cell death discovery · 2024Article
- MicroRNAs as the critical regulators of epithelial mesenchymal transition in pancreatic tumor cells.Heliyon · 2024Review
- Entecavir: A Review and Considerations for Its Application in Oncology.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Review
- Post-translational modifications of histones: Mechanisms, biological functions, and therapeutic targets.MedComm · 2023Review
- Knockdown of KDM5B Leads to DNA Damage and Cell Cycle Arrest in Granulosa Cells via MTF1.Current issues in molecular biology · 2023Article
- The KDM5B and KDM1A lysine demethylases cooperate in regulating androgen receptor expression and signalling in prostate cancer.Frontiers in cell and developmental biology · 2023Article
- KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic.Advances in experimental medicine and biology · 2023Article
- Review
- Article
- KDM5B promotes tumorigenesis of Ewing sarcoma via FBXW7/CCNE1 axis.Cell death & disease · 2022Article
- HumanInternational journal of biological sciences · 2022Article
- CG7379 and ING1 suppress cancer cell invasion by maintaining cell-cell junction integrity.Open biology · 2021Article
- Hypoxia Stimulates SUMOylation-Dependent Stabilization of KDM5B.Frontiers in cell and developmental biology · 2021Article
- MiR-374b-5p inhibits KDM5B-induced epithelial-mesenchymal transition in pancreatic cancer.American journal of cancer research · 2021Article
- Mechanisms of JARID1B Up-Regulation and Its Role inFrontiers in oncology · 2021Article
- MicroRNA let-7i Inhibits Histone Lysine Demethylase KDM5B to Halt Esophageal Cancer Progression.Molecular therapy. Nucleic acids · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigenetic alterations such as aberrant expression of histone-modifying enzymes have been implicated in tumorigenesis. KDM5B (also known as JARID1B) is a newly identified histone demethylase that regulates chromatin structure or gene expression by removing methyl residues from trimethylated lysine 4 on histone H3. Recent observations have shown oncogenic activity of KDM5B. However, the role of KDM5B in gastric cancer carcinogenesis remains unclear. In this study, we aimed to investigate the role of KDM5B in gastric cancer. Immunohistochemical analysis, western blotting, and qRT-PCR were used to measure the levels of KDM5B in gastric cancer cell lines, 45 pairs of gastric cancer tissues and the adjacent nonneoplastic tissues. KDM5B and shKDM5B were transfected into gastric cancer cells to investigate its role on regulating cell proliferation which was measured by MTT and colony formation assay. Cell's migration and invasion were measured by Transwell and Matrigel analysis in vitro. PCNA expression was measured by immunofluorescence staining and immunohistochemical analysis. The in vivo tumorigenesis and metastasis assays were performed in SCID mice. In clinical gastric cancer samples, we found that KDM5B expression was significantly up-regulated in cancer lesions compared with paired normal gastric tissues. By silencing or overexpressing KDM5B in gastric cancer cells, we found that KDM5B could promote cell growth and metastasis in vitro. An in vivo assay showed that KDM5B not only dramatically promoted gastric cancer cell xenograft formation and growth but also promoted gastric cancer cell metastasis in a liver metastasis model. Moreover, we demonstrated that KDM5B promoted gastric cancer metastasis via regulation of the Akt pathway. Our study provided evidence that KDM5B functions as a novel tumor oncogene in gastric cancer and may be a potential therapeutic target for gastric cancer management.
Indexed as
Identifiers
25628922PMC4300698W1573393350What OpenQuestion holds
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.