ArticleJournal of molecular cell biology2017
Dysbindin promotes progression of pancreatic ductal adenocarcinoma via direct activation of PI3K.
Article in Journal of molecular cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 24 citations in OpenAlex.
- Dysbindin Domain-Containing 1 in Prostate Cancer: New Insights into Bioinformatic Validation of Molecular and Immunological Features.International journal of molecular sciences · 2023Article
- Application of Proteomics in Pancreatic Ductal Adenocarcinoma Biomarker Investigations: A Review.International journal of molecular sciences · 2022Review
- S100A16 promotes metastasis and progression of pancreatic cancer through FGF19-mediated AKT and ERK1/2 pathways.Cell biology and toxicology · 2021Article
- Association of dysbindin expression with individualized postoperative prognosis and chemotherapy benefit among patients with gastric adenocarcinoma.Journal of Cancer · 2021Article
- Dysbindin facilitates invasion and metastasis by promoting phosphorylation of ERK in epithelial ovarian cancer.Journal of Cancer · 2020Article
- CILP-2 is a novel secreted protein and associated with insulin resistance.Journal of molecular cell biology · 2019Article
- Holliday junction recognition protein interacts with and specifies the centromeric assembly of CENP-T.The Journal of biological chemistry · 2019Article
- Dynamic acetylation of the kinetochore-associated protein HEC1 ensures accurate microtubule-kinetochore attachment.The Journal of biological chemistry · 2019Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) represents a biggest challenge in clinic oncology due to its invasiveness and lack of targeted therapeutics. Our recent study showed that schizophrenia susceptibility factor dysbindin exhibited significant higher level in serum of PDAC patients. However, the functional relevance of dysbindin in PDAC is still unclear. Here, we show that dysbindin promotes tumor growth both in vitro and in vivo by accelerating the G1/S phase transition in cell cycle via PI3K/AKT signaling pathway. Mechanistically, dysbindin interacts with PI3K and stimulates the kinase activity of PI3K. Moreover, overexpression of dysbindin in PDAC is correlated with clinicopathological characteristics significantly, such as histological differentiation (P = 0.011) and tumor size (P = 0.007). Kaplan-Meier survival curves show that patients with high dysbindin expression exhibit poorer overall survival, compared to those with low dysbindin expression (P < 0.001). Multivariate analysis reveals that dysbindin is an independent prognostic factor for pancreatic ductal adenocarcinoma (P = 0.001). Thus, our findings reveal that dysbindin is a novel PI3K activator and promotes PDAC progression via stimulation of PI3K/AKT. Dysbindin therefore represents a potential target for prognosis and therapy of PDAC.
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Registered trials
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