ArticleAnnals of translational medicine2021
Inhibition of bone morphogenetic protein receptor 2 suppresses pancreatic ductal adenocarcinoma growth by regulating GRB2/PI3K/AKT axis.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Computational design and molecular characterization of a multi-epitope peptide vaccine targeting pancreatic cancer.Journal, genetic engineering & biotechnology · 2026Article
- Proteomics in pancreatic cancer.Biomarker research · 2025Review
- A Comprehensive Review Exploring the Role of Bone Morphogenetic Proteins [BMP]: Biological Mechanisms.Current issues in molecular biology · 2025Review
- miR-889-3p targeting BMPR2 promotes the development of retinoblastoma via JNK/MAPK/ERK signaling.Scientific reports · 2024Article
- Discovery of Highly Potent and BMPR2-Selective Kinase Inhibitors Using DNA-Encoded Chemical Library Screening.Journal of medicinal chemistry · 2023Article
- Mechanistic and functional extrapolation of SET and MYND domain-containing protein 2 to pancreatic cancer.World journal of gastroenterology · 2022Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBone morphogenetic protein receptor 2 (BMPR2) is an important transmembrane serine/threonine kinase that involves oncogenic processes in multiple cancers. However, the role of BMPR2 and its regulatory mechanism in pancreatic ductal adenocarcinoma (PDAC) remain unknown.
methodsWe performed a tissue array to explore the expression of BMPR2 in PDAC tissues. The Cell Counting Kit-8 (CCK-8) and colony formation assays were used to measure PDAC cells' proliferation. Proteomics and mass spectrometry technology was applied to analyze the BMPR2-regulating proteins. Flow cytometry was used to analyze the cell cycle distribution of PDAC cells. Orthotopic pancreatic cancer (PC) and patient-derived xenograft (PDX) models were used for
resultsThis study revealed the over-expression of BMPR2 in PDAC tissues and its proliferation-promoting role in PDAC cells. By carrying out protein mass spectrometry technique as well as bioinformatics analysis, we identified that BMPR2 regulated the growth factor receptor-bound protein 2/phosphatidylinositol 3-kinase/protein kinase B (GRB2/PI3K/AKT) signaling pathway, and further in vitro experiments showed that inhibition of BMPR2 resulted in suppressing proliferation and G2/M arrest by inhibiting the GRB2/PI3K/AKT signaling pathway in PDAC cells. The inhibition of BMPR2 by LDN193189 showed similar results in PDAC cells, orthotopic PC, and PDX models, which revealed that inhibition of BMPR2 significantly suppressed tumor growth by suppressing the GRB2/PI3K/AKT axis.
conclusionsInhibition of BMPR2 suppresses PDAC growth by regulating the GRB2/PI3K/AKT axis and is a promising PDAC treatment strategy.
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