RNA Methyltransferase 3 Drives Pancreatic Acinar Cell Carcinoma Growth and Is a Therapeutic Target (STTT, 2026)
In collaboration with our laboratory, Dr. Tatekawa and colleagues used KRAS-independent pancreatic acinar cell carcinoma (ACC) as a natural experiment to uncover METTL3-mediated m⁶A RNA methylation as a fundamental epitranscriptomic dependency of pancreatic tumorigenesis. Genetic and pharmacological inhibition of METTL3 induced rapid tumor apoptosis, highlighting METTL3 as a compelling therapeutic vulnerability and a potential target for combination chemoradiotherapy, while positioning ACC as a unique biological lens through which previously hidden dependencies of pancreatic cancer can be revealed.

