SNHG10 promotes tumorigenesis through the EGFR/AKT/ERK/mTOR and miR-150-5p/VEGF-A axis, along with gemcitabine resistance in pancreatic ductal adenocarcinoma - PubMed
6 hours ago
- #Gemcitabine Resistance
- #SNHG10
- #Pancreatic Cancer
- SNHG10 is overexpressed in pancreatic ductal adenocarcinoma (PDAC) and associated with clinical stages.
- Downregulation of SNHG10 reduces cell proliferation, migration, EMT, and induces apoptosis and cell cycle arrest in PDAC cells.
- SNHG10 interacts with miR-150-5p and VEGF-A, where silencing SNHG10 increases miR-150-5p and decreases VEGF-A expression.
- SNHG10 downregulation inhibits the EGFR/AKT/ERK/mTOR and c-MET signaling pathways in vitro and in xenograft models.
- Silencing SNHG10 enhances gemcitabine sensitivity in gemcitabine-resistant PDAC cells and reduces tumor growth in vivo.
- The study suggests SNHG10 as a potential therapeutic target for PDAC tumorigenesis and drug resistance.