ArticleWorld journal of gastroenterology2010
Insulin-like growth factor-I receptor in proliferation and motility of pancreatic cancer.
Article in World journal of gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Molecular Imaging in Pancreatic Cancer: Current Applications and Future Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Risk of pancreatic cancer according to glycemic status in nonalcoholic fatty liver disease: a nationwide cohort study.Scientific reports · 2025Article
- Bidirectional relationship between pancreatic cancer and diabetes mellitus: a comprehensive literature review.Annals of medicine and surgery (2012) · 2024Review
- Identification of Promising Drug Candidates against Prostate Cancer through Computationally-Driven Drug Repurposing.International journal of molecular sciences · 2023Article
- PDGFR and IGF-1R Inhibitors Induce a G2/M Arrest and Subsequent Cell Death in Human Glioblastoma Cell Lines.Cells · 2018Article
- Exploring the relationship between nonalcoholic fatty liver disease and pancreatic cancer by computed tomographic survey.Internal and emergency medicine · 2018Observational
- Article
- Picropodophyllin (PPP) is a potent rhabdomyosarcoma growth inhibitor both in vitro and in vivo.BMC cancer · 2017Article
- Type I insulin-like growth factor receptor signaling in hematological malignancies.Oncotarget · 2017Review
- Article
- MicroRNA-497 regulates cell proliferation in hepatocellular carcinoma.Oncology letters · 2016Article
- SU11274 suppresses proliferation and motility of pancreatic cancer cells.Oncology letters · 2015Article
- Targeting insulin-like growth factor 1 receptor inhibits pancreatic cancer growth and metastasis.PloS one · 2014Article
- Frizzled-2: A potential novel target for molecular pancreatic cancer therapy.Oncology letters · 2014Article
- Genetic and molecular alterations in pancreatic cancer: implications for personalized medicine.Medical science monitor : international medical journal of experimental and clinical research · 2013Review
- Survival is associated with genetic variation in inflammatory pathway genes among patients with resected and unresected pancreatic cancer.Annals of surgery · 2013Article
- Article
- Niclosamide suppresses Hepatoma cell proliferation via the Wnt pathway.OncoTargets and therapy · 2013Article
- Dual targeting of the insulin-like growth factor and collateral pathways in cancer: combating drug resistance.Cancers · 2011Article
- Emerging therapies in pancreas cancer.Journal of gastrointestinal oncology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo develop a molecular therapy for pancreatic cancer, the insulin-like growth factor-I (IGF-I) signaling pathway was analyzed.
methodsPancreatic cancer cell lines (MIA-Paca2, NOR-P1, PANC-1, PK-45H, PK-1, PK-59 and KP-4) were cultured in media with 10 mL/L fetal bovine serum. Western blotting analysis was performed to clarify the expression of IGF-I receptor (IGF-IR). Picropodophyllin (PPP), a specific inhibitor of IGF-IR, LY294002, a specific inhibitor of phosphatidylinositol 3 kinase (PI3K), and PD98059, a specific inhibitor of mitogen-activated protein kinase, were added to the media. After 72 h, a 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium inner salt (MTS) assay was performed to analyze cell proliferation. A wound assay was performed to analyze cell motility with hematoxylin and eosin (HE) staining 48 h after addition of each inhibitor.
resultsAll cell lines clearly expressed not only IGF-IR but also phosphorylated IGF-IR. PPP significantly suppressed proliferation of MIA-Paca2, NOR-P1, PANC-1, PK-45H, PK-1, PK-59 and KP-4 cells to 36.9% +/- 2.4% (mean +/- SD), 30.9% +/- 5.5%, 23.8% +/- 3.9%, 37.1% +/- 5.3%, 10.4% +/- 4.5%, 52.5% +/- 4.5% and 22.6% +/- 0.4%, at 2 micromol/L, respectively (P < 0.05). LY294002 significantly suppressed proliferation of MIA-Paca2, NOR-P1, PANC-1, PK-45H, PK-1, PK-59 and KP-4 cells to 44.4% +/- 7.6%, 32.9% +/- 8.2%, 53.9% +/- 8.0%, 52.8% +/- 4.0%, 32.3% +/- 4.2%, 51.8% +/- 4.5%, and 30.6% +/- 9.4%, at 50 micromol/L, respectively (P < 0.05). PD98059 did not significantly suppress cell proliferation. PPP at 2 micromol/L suppressed motility of MIA-Paca2, NOR-P1, PANC-1, PK-45H, PK-1, PK-59 and KP-4 cells to 3.0% +/- 0.2%, 0%, 0%, 2.0% +/- 0.1%, 5.0% +/- 0.2%, 3.0% +/- 0.1%, and 5.0% +/- 0.2%, respectively (P < 0.05). LY294002 at 50 micromol/L suppressed motility of MIA-Paca2, NOR-P1, PANC-1, PK-45H, PK-1, PK-59 and KP-4 to 3.0% +/- 0.2%, 0%, 3.0% +/- 0.2%, 0%, 0%, 0% and 3% +/- 0.1%, respectively (P < 0.05). PD980509 at 20 micromol/L did not suppress motility. Cells were observed by microscopy to analyze the morphological changes induced by the inhibitors. Cells in medium treated with 2 micromol/L PPP or 50 micromol/L LY294002 had pyknotic nuclei, whereas those in medium with 20 micromol/L PD98059 did not show apoptosis.
conclusionIGF-IR and PI3K are good candidates for molecular therapy of pancreatic cancer.
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