NIH R01 · 2025
Excessive neutral lipid or fatty acid levels in the tumor microenvironment (TME) are important mechanisms for carcinoma-associated fibroblast (CAF) activation. We showed that lipid reprogramming in CAFs is sustained by increasing lipogenesis mediator, DGAT1, and identified a CAF subtype that appears to have a key specific role in regulating tumor-neural crosstalk and possibly increased innervation and perineural invasion (PNI). We discovered that neural fibroblasts (NF) derived from peripheral nerves become part of the CAF population, can reprogram lipid storage while promoting neuritic-like processes formation, and stimulate tumor progression. To our knowledge, this newly recognized CAF…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.