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NOX1 mediates chemoresistance via HIF1α/MDR1 pathway in gallbladder cancer
Ming Zhan1, Hui Wang1, Tao Chen1
1Department of Biliary-Pancreatic Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Abstract:
NADPH oxidase 1 (NOX1) plays a key role in tumorigenesis and metastasis through generating reactive oxygen species (ROS), an important intracellular signaling molecule. However, how it is expressed in gallbladder cancer (GBC) tissue sample and whether it associates with GBC chemoresistance have never been investigated. Our study analyzed the relationship between NOX1 expression and cisplatin-sensitivity both in vivo and in vitro. We found that reduced NOX1 expression promoted cisplatin efficiency in GBC-SD cells, whereas overexpression of which potentially inhibited the sensitivity of cisplatin in SGC-996 cells. Further study into the mechanism we found that increased NOX1 expression elevated intracellular ROS levels, which then activated HIF-1α/MDR1 pathway. These findings established NOX1 a novel accelerant of chemoresistance in GBC, and NOX1-targeted therapeutics might be exploited as a strategy for increasing the efficacy of cisplatin treatment.
Insights
NADPH oxidase 1 (NOX1) promotes chemoresistance in gallbladder cancer by increasing reactive oxygen species (ROS) and activating the HIF-1α/MDR1 pathway. Targeting NOX1 may enhance cisplatin treatment efficacy.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- NADPH oxidase 1 (NOX1) generates reactive oxygen species (ROS), crucial for cell signaling in tumorigenesis and metastasis.
- The role of NOX1 in gallbladder cancer (GBC) and its association with chemoresistance remain unexplored.
Purpose of the Study:
- To investigate NOX1 expression in GBC tissues.
- To determine the relationship between NOX1 and cisplatin sensitivity in GBC.
- To elucidate the underlying molecular mechanisms of NOX1-mediated chemoresistance.
Main Methods:
- In vivo and in vitro studies using GBC cell lines (GBC-SD and SGC-996).
- Analysis of NOX1 expression levels.
- Measurement of intracellular ROS.
- Investigation of the HIF-1α/MDR1 signaling pathway.
Main Results:
- Reduced NOX1 expression enhanced cisplatin sensitivity in GBC-SD cells.
- Overexpression of NOX1 decreased cisplatin sensitivity in SGC-996 cells.
- Increased NOX1 elevated intracellular ROS, activating the HIF-1α/MDR1 pathway.
Conclusions:
- NOX1 acts as a novel promoter of chemoresistance in gallbladder cancer.
- NOX1-targeted therapies could potentially improve cisplatin treatment efficacy for GBC.
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