FOXD3 Is Functionally Linked to NF‑κB Signaling in KRAS G12C‑Mutant NSCLC Cells
FOXD3 overexpression suppresses malignant phenotypes in two KRAS G12C‑mutant NSCLC models.
The study investigates the role of FOXD3 overexpression in two KRAS G12C‑mutant non‑small cell lung cancer (NSCLC) cell lines, SW1573 and LU65. FOXD3 overexpression suppresses malignant phenotypes such as cell viability, migration, invasion and tumour growth in vitro and in vivo, and is associated with reduced NF‑κB transcriptional activity. TNF‑α stimulation reverses these effects partially.
FOXD3 may modulate NF‑κB‑dependent signalling and tumour‐survival mechanisms in KRAS G12C‑mutant NSCLC, representing a potential therapeutic target or biomarker.
Evidence level: Sejtvonalas. Laboratóriumi sejtekben vizsgálták.
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