KEY TAKEAWAYS
- The study aimed to investigate GNL3 expression in LUAD and its role in inhibiting LUAD cell growth via potential mechanisms.
- The results concluded that the GNL3 drives LUAD progression through the Wnt/β-catenin axis; targeting GNL3 could be a novel LUAD therapy.
Lung adenocarcinoma (LUAD) is a leading cause of tumor-associated mortality, highlighting the need for new therapeutic targets. Guanine nucleotide-binding protein-like 3 (GNL3) regulates cell proliferation and apoptosis in various cancers, but its role in LUAD is still unclear.
Guihong Dai and the team aimed to investigate the expression and function of GNL3 in LUAD and its mechanism in inhibiting LUAD cell growth.
Researchers evaluated GNL3 expression in LUAD tissues and its association with patient prognosis using databases and immunohistochemistry. They assessed cell proliferation through CCK-8 assay and colony formation, and evaluated apoptosis via flow cytometry. The effect of GNL3 knockdown on the Wnt/β-catenin axis was examined using immunoblot analysis.
The results showed that GNL3 is overexpressed in LUAD tissues and correlates with poor prognosis. Knockdown of GNL3 significantly inhibited growth and induced apoptosis in A549 and H1299 cells. Additionally, the inhibitory effect of GNL3 knockdown on LUAD cell growth was associated with downregulation of the Wnt/β-catenin axis.
No funding information was available.
Source: https://pubmed.ncbi.nlm.nih.gov/38970264/
Dai G, Sun Y. (2024). “Knockdown of GNL3 inhibits LUAD cell growth by regulating Wnt-β-catenin pathway.” Allergol Immunopathol (Madr). 2024;52(4):46-52. Published 2024 Jul 1. doi:10.15586/aei.v52i4.1117
