Neobractatin and Trametinib Synergistically Induce Apoptosis and Gasdermin E‐Dependent Pyroptosis in Pancreatic Cancer Cells

ABSTRACT Mutations in mitogen‐activated protein kinase kinase (MEK) are prevalent in pancreatic ductal adenocarcinoma (PDAC), but many MEK inhibitors inadvertently activate protein kinase B (AKT). We propose a promising PDAC treatment strategy by combining the MEK inhibitor trametinib with neobracta...

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Main Authors: Jiaqi Tan, Ziyi Bao, Kai Qin, Liujing Zhu, Changwu Zheng, Jiabin Jin, Li Zhang, Hongxi Xu
Format: Article
Language:English
Published: Wiley 2025-07-01
Series:MedComm
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Online Access:https://doi.org/10.1002/mco2.70250
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author Jiaqi Tan
Ziyi Bao
Kai Qin
Liujing Zhu
Changwu Zheng
Jiabin Jin
Li Zhang
Hongxi Xu
author_facet Jiaqi Tan
Ziyi Bao
Kai Qin
Liujing Zhu
Changwu Zheng
Jiabin Jin
Li Zhang
Hongxi Xu
author_sort Jiaqi Tan
collection DOAJ
description ABSTRACT Mutations in mitogen‐activated protein kinase kinase (MEK) are prevalent in pancreatic ductal adenocarcinoma (PDAC), but many MEK inhibitors inadvertently activate protein kinase B (AKT). We propose a promising PDAC treatment strategy by combining the MEK inhibitor trametinib with neobractatin (NBT), a natural compound from Garcinia bracteata. Our results demonstrated that this combination significantly impeded cell growth by inducing gasdermin E (GSDME)‐mediated pyroptosis and apoptosis. GSDME, overexpressed in PDAC tissues and correlated with histological differentiation, underscores the role of pyroptosis in PDAC. RNA‐seq results indicated that the phosphoinositide 3‐kinase/protein kinase B (PI3K/AKT) pathway was the primary target of the combination treatment. Mechanistic studies revealed the combination effectively reduced both total and phosphorylated AKT levels, thereby inhibiting protein kinase B/IκB kinase (AKT/IKK) and protein kinase B/mammalian target of rapamycin (AKT/mTOR) signaling pathways. Additionally, the combination disrupted mTOR complex 2 (mTORC2), preventing the trametinib‐induced AKT activation. MicroRNA sequencing analysis indicated that the combination reduced AKT levels by upregulated miR‐149‐5p. Further research demonstrated that the combination increased intracellular reactive oxygen species (ROS), while N‐acetylcysteine (NAC, a ROS scavenger) reversed the cell growth inhibition and AKT suppression. In vivo, the combination significantly inhibited tumor growth by inducing pyroptosis and apoptosis, outperforming gemcitabine. Our findings provide novel insights into the potential of combining NBT and trametinib to induce pyroptosis and apoptosis through the ROS/AKT/GSDME axis, offering a theoretical basis for future PDAC treatment.
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spelling doaj-art-89e01ac2c6f941579914265986162e8f2025-08-20T03:50:49ZengWileyMedComm2688-26632025-07-0167n/an/a10.1002/mco2.70250Neobractatin and Trametinib Synergistically Induce Apoptosis and Gasdermin E‐Dependent Pyroptosis in Pancreatic Cancer CellsJiaqi Tan0Ziyi Bao1Kai Qin2Liujing Zhu3Changwu Zheng4Jiabin Jin5Li Zhang6Hongxi Xu7School of PharmacyShanghai University of Traditional Chinese MedicineShanghaiChinaSchool of PharmacyShanghai University of Traditional Chinese MedicineShanghaiChinaDepartment of General SurgeryPancreatic Disease CenterRuijin Hospital, Shanghai Jiao Tong University School of MedicineShanghaiChinaSchool of PharmacyShanghai University of Traditional Chinese MedicineShanghaiChinaSchool of PharmacyShanghai University of Traditional Chinese MedicineShanghaiChinaDepartment of General SurgeryPancreatic Disease CenterRuijin Hospital, Shanghai Jiao Tong University School of MedicineShanghaiChinaSchool of PharmacyShanghai University of Traditional Chinese MedicineShanghaiChinaShuguang Hospital, Shanghai University of Traditional Chinese MedicineShanghaiChinaABSTRACT Mutations in mitogen‐activated protein kinase kinase (MEK) are prevalent in pancreatic ductal adenocarcinoma (PDAC), but many MEK inhibitors inadvertently activate protein kinase B (AKT). We propose a promising PDAC treatment strategy by combining the MEK inhibitor trametinib with neobractatin (NBT), a natural compound from Garcinia bracteata. Our results demonstrated that this combination significantly impeded cell growth by inducing gasdermin E (GSDME)‐mediated pyroptosis and apoptosis. GSDME, overexpressed in PDAC tissues and correlated with histological differentiation, underscores the role of pyroptosis in PDAC. RNA‐seq results indicated that the phosphoinositide 3‐kinase/protein kinase B (PI3K/AKT) pathway was the primary target of the combination treatment. Mechanistic studies revealed the combination effectively reduced both total and phosphorylated AKT levels, thereby inhibiting protein kinase B/IκB kinase (AKT/IKK) and protein kinase B/mammalian target of rapamycin (AKT/mTOR) signaling pathways. Additionally, the combination disrupted mTOR complex 2 (mTORC2), preventing the trametinib‐induced AKT activation. MicroRNA sequencing analysis indicated that the combination reduced AKT levels by upregulated miR‐149‐5p. Further research demonstrated that the combination increased intracellular reactive oxygen species (ROS), while N‐acetylcysteine (NAC, a ROS scavenger) reversed the cell growth inhibition and AKT suppression. In vivo, the combination significantly inhibited tumor growth by inducing pyroptosis and apoptosis, outperforming gemcitabine. Our findings provide novel insights into the potential of combining NBT and trametinib to induce pyroptosis and apoptosis through the ROS/AKT/GSDME axis, offering a theoretical basis for future PDAC treatment.https://doi.org/10.1002/mco2.70250AKTgasdermin Epancreatic ductal adenocarcinomapyroptosisROS
spellingShingle Jiaqi Tan
Ziyi Bao
Kai Qin
Liujing Zhu
Changwu Zheng
Jiabin Jin
Li Zhang
Hongxi Xu
Neobractatin and Trametinib Synergistically Induce Apoptosis and Gasdermin E‐Dependent Pyroptosis in Pancreatic Cancer Cells
MedComm
AKT
gasdermin E
pancreatic ductal adenocarcinoma
pyroptosis
ROS
title Neobractatin and Trametinib Synergistically Induce Apoptosis and Gasdermin E‐Dependent Pyroptosis in Pancreatic Cancer Cells
title_full Neobractatin and Trametinib Synergistically Induce Apoptosis and Gasdermin E‐Dependent Pyroptosis in Pancreatic Cancer Cells
title_fullStr Neobractatin and Trametinib Synergistically Induce Apoptosis and Gasdermin E‐Dependent Pyroptosis in Pancreatic Cancer Cells
title_full_unstemmed Neobractatin and Trametinib Synergistically Induce Apoptosis and Gasdermin E‐Dependent Pyroptosis in Pancreatic Cancer Cells
title_short Neobractatin and Trametinib Synergistically Induce Apoptosis and Gasdermin E‐Dependent Pyroptosis in Pancreatic Cancer Cells
title_sort neobractatin and trametinib synergistically induce apoptosis and gasdermin e dependent pyroptosis in pancreatic cancer cells
topic AKT
gasdermin E
pancreatic ductal adenocarcinoma
pyroptosis
ROS
url https://doi.org/10.1002/mco2.70250
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