ArticleMolecular and cellular biochemistry2015
Insulin-like growth factor binding protein-3 enhances etoposide-induced cell growth inhibition by suppressing the NF-κB activity in gastric cancer cells.
Article in Molecular and cellular biochemistry, 2015. 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, 15 citations in OpenAlex.
- Insulin‑like growth factor in cancer: New perspectives (Review).Molecular medicine reports · 2025Review
- IGFBP3 modulation of tumor pathogenesis and cell signaling pathways (Review).Oncology letters · 2025Review
- The role of IGFBP-3 in tumor development and progression: enlightenment for diagnosis and treatment.Medical oncology (Northwood, London, England) · 2024Review
- Inhibition of Chitinase-3-like-1 by K284-6111 Reduces Atopic Skin Inflammation via Repressing Lactoferrin.Immune network · 2021Article
- DNMT3A-mediated silence in ADAMTS9 expression is restored by RNF180 to inhibit viability and motility in gastric cancer cells.Cell death & disease · 2021Article
- Insulin-like growth factor binding protein 3 promotes radiosensitivity of oral squamous cell carcinoma cells via positive feedback on NF-κB/IL-6/ROS signaling.Journal of experimental & clinical cancer research : CR · 2021Article
- The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia.Frontiers in cell and developmental biology · 2021Review
- Recombinant human insulin-like growth factor binding protein 3 attenuates lipopolysaccharide-induced acute lung injury in mice.International journal of clinical and experimental pathology · 2020Article
- NF-κB Signaling in Gastric Cancer.Toxins · 2017Review
- COMP-Ang1 enhances DNA synthesis and cell cycle progression in human periodontal ligament cells via Tie2-mediated phosphorylation of PI3K/Akt and MAPKs.Molecular and cellular biochemistry · 2016Article
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2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear factor-kappaB (NF-κB) is a transcription factor that is activated in various neoplasms, including gastric cancer. Insulin-like growth factor binding protein-3 (IGFBP-3) is a potent tumor suppressor and is significantly suppressed in a variety of cancers. Although IGFBP-3 has been reported to have antiproliferative and proapoptotic effects, the precise mechanisms underlying the action of IGFBP-3 have not been elucidated. In this study, we found an inverse correlation between NF-κB activity and IGFBP-3 expression in patients with gastric cancer. Overexpression of IGFBP-3 resulted in significant inhibition of total and phosphorylated p65 NF-κB and IκB proteins in gastric cancer cells. IGFBP-3 further inhibited the expression of NF-κB-regulated cell adhesion molecules, ICAM-1 and VCAM-1. Finally, the growth inhibition induced by etoposide was significantly enhanced by IGFBP-3 overexpression along with concomitant suppression of NF-κB activity. These findings indicate that IGFBP-3 enhances etoposide-induced cell growth inhibition by blocking the NF-κB signaling pathway in gastric cancer cells. Furthermore, our data suggest that IGFBP-3 could be used as an adjuvant in the treatment of gastric cancer.
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