ArticleMolecular and cellular biochemistry2025
PCSK5 downregulation promotes the inhibitory effect of andrographolide on glioblastoma through regulating STAT3.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Traditional Chinese Medicine-Derived Active Ingredient and Formulation Therapy for Glioma: Multi-Target Mechanisms, Drug Delivery Systems, and Advances in Clinical Translational Research.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Identification and validation of a Golgi apparatus related gene signature for prognosis prediction and immune microenvironment profiling in colorectal cancer.Discover oncology · 2026Article
- Prognostic value of brown adipocyte-related genes in colorectal cancer: a multi-omics and Mendelian randomization study.Discover oncology · 2025Article
- PDGF-D Promotes Epithelial-Mesenchymal Transition of Glioma Cells Through the NF-κB/NOTCH1 Pathway.Cancer medicine · 2025Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Proprotein convertase subtilisin/kexin type 5 (PCSK5) is a member of the proprotein convertase (PC) family, which processes immature proteins into functional proteins and plays an important role in the process of cell migration and transformation. Andrographolide is a non-peptide compound with PC inhibition and antitumor activity. Our research aimed to investigate the functional role of PCSK5 downregulation combined with Andro on GBM progression. Results from the cancer genome atlas (TCGA) and clinical samples revealed a significant upregulation of PCSK5 in GBM tissues than in non-tumor brain tissues. Higher expression of PCSK5 was correlated with advanced GBM stages and worse patient prognosis. PCSK5 knockdown attenuated the epithelial-mesenchymal transition (EMT)-like properties of GBM cells induced by IL-6. PCSK5 knockdown in combination with Andro treatment significantly inhibited the proliferation and invasion of GBM cells in vitro, as well as tumor growth in vivo. Mechanistically, PCSK5 downregulation reduced the expression of p-STAT3 and Matrix metalloproteinases (MMPs), which could be rescued by the p-STAT3 agonist. STAT3 silencing downregulated the expression of MMPs without affecting PCSK5. Furthermore, Andro in combination with PCSK5 silencing significantly inhibited STAT3/MMPs axis. These observations provided evidence that PCSK5 functioned as a potential tumor promoter by regulating p-STAT3/MMPs and the combination of Andro with PCSK5 silencing might be a good strategy to prevent GBM progression.
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