Histopathology of pancreatic ductal adenocarcinoma. Singh, P. et al. CC BY 4.0, via Wikimedia Commons
Pancreatic cancer is among the deadliest malignancies, in part because it resists many standard treatments. A new study1 now identifies a previously underappreciated player that helps tumours grow and evade therapy.
Researchers report that a long non-coding RNA molecule, SNHG10, is markedly overexpressed in pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer. Analysing patient samples and cancer cell lines, the team found that higher levels of SNHG10 are linked to more advanced disease.
When the researchers silenced SNHG10 in cancer cells, tumour growth slowed dramatically. Cells showed reduced proliferation, migration and invasive behaviour, while undergoing increased cell death and cell-cycle arrest.
Digging deeper, the study reveals how SNHG10 exerts its effects. The molecule forms part of a regulatory network involving a microRNA (miR-150-5p) and a key growth factor (VEGF-A). By suppressing the microRNA, SNHG10 allows VEGF-A levels to rise — promoting tumour growth and survival.
At the same time, SNHG10 activates major cancer-driving signalling pathways, including EGFR, AKT and mTOR. These pathways are known to support tumour progression and are frequently targeted in cancer therapy.
Importantly, reducing SNHG10 levels also made cancer cells more sensitive to gemcitabine, a frontline chemotherapy drug for pancreatic cancer. In mouse models, tumours lacking SNHG10 were smaller and grew more slowly.
The findings position SNHG10 as a central regulator of both tumour growth and drug resistance. Targeting this RNA molecule, or the pathways it controls, could offer a new strategy for tackling one of the most treatment-resistant cancers.
