ArticleMolecular cancer2025
Non-canonical ALK7 pathways promote pancreatic cancer metastasis through β-catenin/MMP-mediated basement membrane breakdown and intravasation.
Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Metabolites and cancer metastasis.Oncogene · 2026Review
- Nanomedicine targeting ECM stiffness: restoring mechanical homeostasis for cancer immunotherapy.Materials today. Bio · 2026Review
- Lysosomal lipid metabolism promotes tumor cell invasion through local energetics and membrane lipid remodeling.bioRxiv : the preprint server for biology · 2026Article
- Dual-transferred atmospheric-pressure plasma jet modulates matrix metalloproteinase expression in breast cancer stem cells.Biochemistry and biophysics reports · 2026Article
- A paracrine-to-autocrine shunt of GREM1 fuels colorectal cancer metastasis via ACVR1C.Molecular cancer · 2026Article
- LncRNA NKILA as a key regulator in cancer pathogenesis: insights into its mechanisms and clinical implications.Cancer cell international · 2026Review
- Analysis of the SH3-Domain Kinase Binding Protein 1 Predictive Model for Pancreatic Ductal Adenocarcinoma and CCCTC-Binding Factor Transcriptional Regulatory Study.World journal of oncology · 2025Article
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Authors and funding
15 authors.
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Abstract
Breaching the vascular barrier is a critical step in pancreatic ductal adenocarcinoma (PDAC) metastasis, yet the mechanisms enabling this process remain incompletely understood. Transforming growth factor beta (TGFβ) receptors have been extensively studied in many cancer types. However, activin receptor-like kinase 7 (ALK7), one of the TGFβ receptors, is under-investigated, and its roles in PDAC metastasis have been unclear. This study identifies two distinct but interconnected ALK7-driven non-canonical pathways that promote PDAC dissemination. The ALK7-β-catenin-EMT axis enhances intrinsic tumor cell motility, driving epithelial-mesenchymal transition (EMT). In parallel, the ALK7-β-catenin-MMP axis facilitates metastatic invasion by upregulating MMP production, leading to ECM degradation and invadosome formation, which promote vascular barrier breakdown and intravasation. An orthotopic PDAC metastasis model reveals that both pharmacological and genetic ALK7 inhibition suppresses metastasis. 3D microfluidic vessel-on-chip platforms further demonstrate that ALK7 inhibition preserves basement membrane (BM) integrity, limiting intravasation. While MMP inhibition effectively blocks BM breakdown and intravasation, extravasation remains unaffected, highlighting distinct molecular requirements for different metastatic stages. These findings establish ALK7 as a dual-function pro-metastatic regulator that orchestrates both tumor cell plasticity and ECM remodeling, positioning ALK7 inhibition as a promising strategy to target early metastatic dissemination in PDAC.
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