Pancreatic cancer, the name of the disease, hides a serious challenge. In a recent study published in Nature Communications, a group of researchers has discovered an unprecedented approach that may be a crucial step in this challenge. They have made a breakthrough in inhibiting specific enzymes, and this research may bring new light to pancreatic cancer patients.
A recent study suggests that pancreatic cancer progression may be inhibited by inhibition of stromal class I histone deacetylase (HDAC). The findings may provide a new avenue for addressing the challenges posed by pancreatic ductal adenocarcinoma (PDAC).
PDAC is a disease of the refractory tumor microenvironment, and the active matrix causes changes in the pancreatic epithelium, triggering a profibrous response that worsens disease prognosis and enhances drug resistance. This study focused on stromal fibroblasts, specifically pancreatic stellate cells (PSCs), which are essential for the development of PDAC.
The researchers found that by inhibiting class I HDACs, such as entinostat (ENT), it was possible to alter the activity of PSCs in vitro. They performed genome-wide analysis of changes in expression and found that inhibition of HDAC altered the activation state of PSC.
In further study, the team also found that HDACI influences the transcription factors or coregulators that drive the pro-fibrous transcriptional pathway. In addition, HDACI also reduced tumor promoting and reduced the severity of PDAC.
This study also demonstrated the validation of HDACI efficacy in vivo and showed the best effect in a mouse PDAC model. Intervention in HDAC appears to alter the properties of stromal fibroblasts, thus affecting the development of PDAC.
The researchers believe that these findings will provide new possibilities for HDAC-based methods and are expected to be an important breakthrough for PDAC. The results of this study provide a new perspective for understanding the mechanism of pancreatic cancer development, and may provide important clues for the development of ** protocols.