ArticleOncotarget2019
IGFBP-2 acts as a tumour suppressor and plays a role in determining chemosensitivity in bladder cancer cells.
Article in Oncotarget, 2019. 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, 13 citations in OpenAlex.
- Loss of protein phosphatase 1 regulator TIMAP protein triggers EMT in A549 cells.Cell communication and signaling : CCS · 2026Article
- IGFBP2 alteration contributes to prostate cancer progression by modulating prostate stroma activation.Cell communication and signaling : CCS · 2025Article
- Integration of Gastric Cancer RNA-Seq Datasets Along With PPI Network Suggests That Nonhub Nodes Have the Potential to Become Biomarkers.Cancer reports (Hoboken, N.J.) · 2025Article
- Evaluation ofResearch in pharmaceutical sciences · 2024Article
- Secreted PGK1 and IGFBP2 contribute to the bystander effect of miR-10b gene editing in glioma.Molecular therapy. Nucleic acids · 2023Article
- Prognostic impact of insulin-like growth factor-I and its binding proteins, insulin-like growth factor-I binding protein-2 and -3, on adverse histopathological features and survival outcomes after radical cystectomy.International journal of urology : official journal of the Japanese Urological Association · 2022Article
- mRNA-miRNA bipartite networks reconstruction in different tissues of bladder cancer based on gene co-expression network analysis.Scientific reports · 2022Article
- The Sirenic Links between Diabetes, Obesity, and Bladder Cancer.International journal of molecular sciences · 2021Review
- Phosphorylation of pericyte FAK-Y861 affects tumour cell apoptosis and tumour blood vessel regression.Angiogenesis · 2021Article
- Potential Role of Insulin Growth-Factor-Binding Protein 2 as Therapeutic Target for Obesity-Related Insulin Resistance.International journal of molecular sciences · 2021Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
There are mixed reports on the role that IGFBP-2 plays in cancer progression, with some indicating a tumour suppressive role and others showing that IGFBP-2 may act as an oncogene. These apparent contradictions may be context and tissue specific. In this study we determined the role that IGFBP-2 played on the phenotype and chemosensitivity of a selection of bladder cancer cell lines and investigated how the abundance of IGFBP-2 was regulated. We found that IGFBP-2 was more abundant in the epithelial bladder cancer cells, RT4 and UMUC3 and absent in the more mesenchymal T24 and TCCSUP cells. Silencing IGFBP-2 using siRNA in epithelial RT4 cells promoted cell proliferation, invasion, colony formation, resulted in a reduction in epithelial (E-cadherin) and an increase in mesenchymal (N-cadherin) markers and increased sensitivity to cisplatin-induced cell death. Conversely, we observed the opposite effects when adding exogenous IGFBP-2 to the mesenchymal T24 cells. We determined that IGFBP-2 was epigenetically silenced via DNA methylation as the cells adopted a mesenchymal phenotype. Collectively these data suggest that IGFBP-2 acts as a tumour suppressor and marker of chemosensitivity in epithelial bladder cancer cells and that IGFBP-2 is epigenetically silenced by methylation to promote bladder cancer 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 OpenQuestion graph.