ArticleAmerican journal of cancer research2022
CKB affects human osteosarcoma progression by regulating the p53 pathway.
Article in American journal of cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Creatine kinase B, a downstream effector of c-Myb, controls migration of osteosarcoma cells via regulation of N-cadherin.Cancer cell international · 2025Article
- Creatine Kinase Blockade Disrupts Energy Metabolism and Redox Homeostasis to Suppress Osteosarcoma Progression.International journal of molecular sciences · 2025Article
- Multi-omics analysis reveals immunosuppression in oesophageal squamous cell carcinoma induced by creatine accumulation and HK3 deficiency.Genome medicine · 2025Article
- Network pharmacology-based research on the effect of angelicin on osteosarcoma and the underlying mechanism.Aging · 2023Article
- Role of creatine shuttle in colorectal cancer cells.Oncotarget · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to explore the role of the creatine kinase B (CKB) gene in the development of human osteosarcoma (OS). Western blotting and qRT-PCR were performed to detect CKB expression in tissues and cells. CCK-8, colony formation, flow cytometry, Transwell, and cell scratch assays were performed to detect OS cell viability, proliferation, apoptosis, invasion, and migration. Gene set enrichment analysis (GSEA) was used to conduct signal pathway enrichment. CKB expression was higher in OS tissues and cells than that in normal tissues and cells. Silencing CKB expression reduced cell proliferation, migration, and invasion, and improved cell apoptosis in HOS cells, while overexpressing CKB increased cell proliferation, migration, and invasion, and decreased apoptosis in U2-OS cells. GSEA showed that CKB affected the p53 signaling pathway. Overexpression of CKB inhibited the protein expression of p53, p21, and Bax and promoted the expression of Bcl-2 and MDM2 in U2-OS cells. Conversely, silencing CKB promoted the protein expression of p53, p21, and Bax, and inhibited the expression of Bcl-2 and MDM2 in HOS cells. Silencing p53 could reverse the effect of the silencing CKB in HOS cells, and overexpressing p53 could reverse the effect of overexpressing CKB in U2-OS cells. Taken together, CKB affects the development of OS by regulating the activity of the p53 signaling pathway.
Indexed as
Identifiers
36381321PMC9641398W4309247654What 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.