ArticleClinical science (London, England : 1979)2025
PDCD10/CCM3, a potential target for pancreatic ductal adenocarcinoma?
Article in Clinical science (London, England : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- The MST4-14-3-3ζ complex promotes pancreatic cancer by activating YAP.Biology direct · 2026Article
- Tumour Cell Size Control and Its Impact on Tumour Cell Function.Cell proliferation · 2025Review
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant progression of pancreatic ductal adenocarcinoma (PDAC) is driven by transforming growth factor (TGF)-β1 through extensive cross-talk with other signalling pathways. Prompted by the observation that the ubiquitous protein programmed cell death 10 (PDCD10) is more abundantly expressed in PDAC tumour tissue compared with normal pancreas and highly correlated with reduced patient survival, authors examined its function as a modulator of TGF-β signalling in PDAC. Cytotoxicity assays with PDAC-derived tumour cell lines, PaTu8902 (DPC4+/+) and PaTu8988t (DPC4-/-) engineered to homozygously lack PDCD10 showed that PDCD10 renders cells more chemoresistant to anticancer drugs. Moreover, PDCD10 promoted TGF-β1-dependent proliferation by inactivating the retinoblastoma 1 protein (pRb) via a SMAD4-dependent pathway, and TGF-β1-driven EMT by increasing ERK1/2 activation via a non-SMAD4 pathway. Phosphorylation of pRB and ERK by PDCD10 is facilitated by binding of PDCD10 to MST4. Targeting PDCD10 in PDAC patients may represent a promising new strategy to improve TGF-β targeted therapies.
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