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KLF5 enables dichotomous lineage programs in pancreatic cancer via the AAA+ ATPase coactivators RUVBL1 and RUVBL2.

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Nature communications 📖 저널 OA 93.2% 2021: 2/2 OA 2022: 3/3 OA 2023: 3/3 OA 2024: 21/21 OA 2025: 202/202 OA 2026: 180/210 OA 2021~2026 2025 Vol.16(1) p. 9996
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Cunniff PJ, Sivetz N, Skopelitis D, Klingbeil O, Toobian D, Maia-Silva D, Egeblad M, Vakoc CR

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Lineage plasticity is a hallmark of pancreatic ductal adenocarcinoma (PDAC) and contributes to tumor heterogeneity and therapeutic resistance.

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APA Cunniff PJ, Sivetz N, et al. (2025). KLF5 enables dichotomous lineage programs in pancreatic cancer via the AAA+ ATPase coactivators RUVBL1 and RUVBL2.. Nature communications, 16(1), 9996. https://doi.org/10.1038/s41467-025-66007-0
MLA Cunniff PJ, et al.. "KLF5 enables dichotomous lineage programs in pancreatic cancer via the AAA+ ATPase coactivators RUVBL1 and RUVBL2.." Nature communications, vol. 16, no. 1, 2025, pp. 9996.
PMID 41241675 ↗

Abstract

Lineage plasticity is a hallmark of pancreatic ductal adenocarcinoma (PDAC) and contributes to tumor heterogeneity and therapeutic resistance. Here, we identify KLF5 as a dynamic master regulator of epithelial lineage identity in PDAC, with dichotomous roles in promoting either classical or basal-like transcriptional programs. Through unbiased proteomic and genetic screens, we uncover the AAA+ ATPases RUVBL1 and RUVBL2 as essential coactivators of KLF5 across both lineage states. We demonstrate that ATP hydrolysis by RUVBL1/2 is required for the stable interaction with an intrinsically disordered region of KLF5, enabling its recruitment to lineage-specific enhancers and driving transcriptional regulation of identity-defining genes. Notably, small-molecule inhibitors of RUVBL1/2 ATPase activity, which have anti-PDAC activity in vivo, suppress KLF5-dependent transcription. These findings define a previously unrecognized mechanism of ATP hydrolysis-dependent transcriptional coactivation and highlight a potential therapeutic strategy for modulating aberrant lineage programs in cancer.

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