TY - JOUR
T1 - Discovery of a novel STAT3 inhibitor
T2 - A potential application for pancreatic cancer treatment
AU - Yang, Xiaoyu
AU - Hung, Chia Nung
AU - Ybarra, Meagan
AU - Villarreal, Michelle
AU - Osmulski, Pawel
AU - Gaczynska, Maria E.
AU - Selvam, Chelliah
AU - Li, Danmeng
AU - Kho, Kenneth L.
AU - Halff, Glenn A.
AU - Ostrov, David A.
AU - Ghosh, Rita
AU - Kumar, Addanki P.
N1 - Publisher Copyright:
© 2025 The Authors
PY - 2025/10
Y1 - 2025/10
N2 - Pancreatic ductal adenocarcinoma (PDAC) is projected to become the second leading cause of cancer-related deaths by 2030, with most patients presenting with advanced, unresectable disease. Despite advances in chemotherapy, the 5-year survival rate remains low, underscoring the need for novel therapies. This study builds on the discovery that palmatine, a natural compound inhibits pancreatic cancer growth and enhances gemcitabine efficacy. This was done by using computational docking to explore palmatine's interaction with the STAT3 linker domain. A screening of 139,735 compounds from the National Cancer Institute Developmental Therapeutics Program identified compounds with superior STAT3 binding, with Striatal B emerging as the lead. In vitro tests confirmed the ability of Striatal B to significantly inhibit pancreatic cancer cell growth and potentiate gemcitabine effects, while computational modeling indicated effective binding to STAT3. Striatal B reduced STAT3 activation and epithelial-mesenchymal transition markers and modulated mechanical properties, suggesting a mechanism of action that involves altering cell mechanics, potentially providing a promising new therapeutic avenue for PDAC treatment.
AB - Pancreatic ductal adenocarcinoma (PDAC) is projected to become the second leading cause of cancer-related deaths by 2030, with most patients presenting with advanced, unresectable disease. Despite advances in chemotherapy, the 5-year survival rate remains low, underscoring the need for novel therapies. This study builds on the discovery that palmatine, a natural compound inhibits pancreatic cancer growth and enhances gemcitabine efficacy. This was done by using computational docking to explore palmatine's interaction with the STAT3 linker domain. A screening of 139,735 compounds from the National Cancer Institute Developmental Therapeutics Program identified compounds with superior STAT3 binding, with Striatal B emerging as the lead. In vitro tests confirmed the ability of Striatal B to significantly inhibit pancreatic cancer cell growth and potentiate gemcitabine effects, while computational modeling indicated effective binding to STAT3. Striatal B reduced STAT3 activation and epithelial-mesenchymal transition markers and modulated mechanical properties, suggesting a mechanism of action that involves altering cell mechanics, potentially providing a promising new therapeutic avenue for PDAC treatment.
UR - https://www.scopus.com/pages/publications/105014653874
UR - https://www.scopus.com/pages/publications/105014653874#tab=citedBy
U2 - 10.1016/j.biopha.2025.118487
DO - 10.1016/j.biopha.2025.118487
M3 - Article
C2 - 40885146
AN - SCOPUS:105014653874
SN - 0753-3322
VL - 191
JO - Biomedicine and Pharmacotherapy
JF - Biomedicine and Pharmacotherapy
M1 - 118487
ER -