Reduced expression of annexin A1 promotes gemcitabine and 5-fluorouracil drug resistance of human pancreatic cancer.
Qing-Hua LiuHong-Mei YongQing-Xin ZhuangXu-Ping ZhangPing-Fu HouYan-Su ChenMing-Hua ZhuJin BaiPublished in: Investigational new drugs (2019)
Intrinsic chemoresistance is the main reason for the failure of human pancreatic ductal adenocarcinoma (PDAC) therapy. To identify the candidate protein, we compared the protein expression profiling of PDAC cells and its distinct surviving cells following primary treatment with gemcitabine (GEM) and 5-fluorouracil (5-FU) by two-dimensional electrophoresis combined with liquid chromatography-mass spectrometry or mass spectrometry. A total of 20 differentially expressed proteins were identified, and annexin A1 (ANXA1) was analyzed for further validation. The functional validation showed that the downregulation of ANXA1 contributes to GEM and 5-FU resistance in PDAC cells through protein kinase C/c-Jun N-terminal kinase/P-glycoprotein signaling pathway. Our findings provide a platform for the further elucidation of the underlying mechanisms of PDAC intrinsic chemoresistance and demonstrated that ANXA1 may be a valid marker for anticancer drug development.
Keyphrases
- induced apoptosis
- mass spectrometry
- signaling pathway
- liquid chromatography
- cell cycle arrest
- endothelial cells
- protein kinase
- pi k akt
- endoplasmic reticulum stress
- oxidative stress
- high resolution
- cell death
- epithelial mesenchymal transition
- stem cells
- capillary electrophoresis
- poor prognosis
- high throughput
- gene expression
- high performance liquid chromatography
- gas chromatography
- locally advanced
- radiation therapy
- dna methylation
- long non coding rna
- simultaneous determination