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This research investigates KMT2D's role as an epigenetic regulator in lung squamous cell carcinoma and its effect on lineage plasticity.

KMT2D Regulates Lineage Plasticity in Lung Squamous Cell Carcinoma

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Findings demonstrate KMT2D's role in inducing lineage plasticity in lung squamous cell carcinoma, highlighting therapeutic implications.

This research investigates KMT2D's role as an epigenetic regulator in lung squamous cell carcinoma and its effect on lineage plasticity.
Utilized mouse lung cancer models (Pik3caH1047R/p53-/- and KrasMut/p53-/-) to evaluate Kmt2d's role.
Employed single-nuclei multiomics profiling (snRNA-seq and snATAC-seq) for tumor cell analysis.
Conducted ChIP-seq and CUT&RUN for key histone marks and transcription factors.
Kmt2d loss promoted lineage transition to squamous identity and accelerated tumor growth.
Single-nuclei analysis showed disruption of endodermal differentiation programs due to Kmt2d deficiency.
Regions activated in Kmt2d-null tumors were enriched for chromatin remodelers and oncogenes like NFE2L2.

Jiang et al. (2026) studied this question.

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