scholarly journals High Expression of FAM83B Predicts Poor Prognosis in Patients with Pancreatic Ductal Adenocarcinoma and Correlates with Cell Cycle and Cell Proliferation

2017 ◽  
Vol 8 (16) ◽  
pp. 3154-3165 ◽  
Author(s):  
Chao-qin Shen ◽  
Ting-Ting Yan ◽  
Wei Liu ◽  
Xiao-qiang Zhu ◽  
Xiang-long Tian ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Poor Prognosis ◽  
High Expression ◽  
Ductal Adenocarcinoma

High expression of ErbB3 binding protein 1 (EBP1) predicts poor prognosis of pancreatic ductal adenocarcinoma (PDAC)

Tumor Biology ◽  
2015 ◽  
Vol 36 (12) ◽  
pp. 9189-9199 ◽  
Author(s):  
Chen Gong ◽  
Yixin Zhang ◽  
Yinji Chen ◽  
Haifeng Zhang ◽  
Xiaorong Liu ◽  
...  
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Poor Prognosis ◽  
Binding Protein ◽  
High Expression ◽  
Ductal Adenocarcinoma

scholarly journals KIF4A Regulates the Progression of Pancreatic Ductal Adenocarcinoma through Proliferation and Invasion

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jing Chen ◽  
Cui-Cui Zhao ◽  
Fei-Ran Chen ◽  
Guo-Wei Feng ◽  
Fei Luo ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Disease Free Survival ◽  
High Expression ◽  
Ductal Adenocarcinoma ◽  
Migration And Invasion

Background. Pancreatic cancer is a malignant tumor of the digestive tract, which is difficult to diagnose and treat due to bad early diagnosis. We aimed to explore the role of kinesin superfamily 4A (KIF4A) in pancreatic ductal adenocarcinoma (PDAC). Methods. We first used the bioinformatic website to screen the data of pancreatic cancer in TCGA, and KIF4A protein was detected among the 86 specimens of patients in our hospital combined with clinic-pathological characteristics and survival analysis. KIF4A loss-expression cell lines were established by RNA interference (RNAi). In addition, we performed in vitro cell assays to detect the changes in cell proliferation, migration, and invasion. The proteins involved in the proliferation and metastasis of cancer cells were also detected by western blot. The above results could be proved in vivo. Further, the correlation between KIF4A and CDC5L was analyzed by TCGA and IHC data. Results. We first found a high expression of KIF4A in pancreatic cancer, suggesting a role of KIF4A in the development of pancreatic cancer. KIF4A was found to be differentially expressed ( P < 0.05 ) among the 86 specimens of patients in our hospital and was significantly associated with PDAC TNM stages and tumor size. High KIF4A expression also significantly worsened overall survival (OS) and disease-free survival rate (DFS) ( P < 0.05 , respectively). In addition, cell proliferation, migration, and invasion were inhibited by the KIF4A-shRNA group compared with the control ( P < 0.05 , respectively). In the end, knockdown of KIF4A could inhibit tumor development and metastasis in vivo. Further, the positive correlation between KIF4A and CDC5L existed, and KIF4A might promote pancreatic cancer proliferation by affecting CDC5L expression. Conclusion. In conclusion, the high expression level of KIF4A in PDAC was closely related to poor clinical and pathological status, lymphatic metastasis, and vascular invasion. KIF4A might be involved in promoting the development of PDAC in vitro and in vivo, which might be a new therapeutic target of PDAC.

SLC39A1 Contributes to Gemcitabine Resistance of Pancreatic Ductal Adenocarcinoma by Activating AMPK Signaling

2021 ◽  
Author(s):  
Hao Yu ◽  
Xiaoping Mei ◽  
Xueming Zhang ◽  
Neng Qian ◽  
Qingjiang Yu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Western Blotting ◽  
Poor Prognosis ◽  
Ductal Adenocarcinoma ◽  
Tumor Type ◽  
Ampk Signaling ◽  
Gemcitabine Resistance ◽  
Mrna And Protein Expression

Abstract Objective: Pancreatic ductal adenocarcinoma (PDAC) serves as a prevailing tumor type with high mortality and poor prognosis. The study aims to explore the mechanism of gemcitabine resistance in PDAC patients. Methods: Immunohistochemistry(IHC)was used to analyze the expression of SLC39A1 in PDAC samples. PDAC cells were culture and transfected with siSLC39A1 and siNC, respectively. Cell proliferation analysis was performed using CCK-8 assay. And qPCR and Western blotting was used to analysis the expression level of SLC39A1 and related signal molecular in cells. Results: IHC results demonstrated that the SLC39A1 expression was significantly up-regulated in the gemcitabine-resistant PDAC samples compared with gemcitabine-sensitive PDAC samples. The treatment of gemcitabine dose-dependently inhibited the viability of the PDAC cells. Meanwhile, the mRNA and protein expression of SLC39A1 were elevated in the gemcitabine-resistant PDAC. The treatment of gemcitabine remarkably decreased viability of PDACs, in which SLC39A1 depletion could reverse this effect. SLC39A1 knockdown could reverse the gemcitabine-induced phosphorylation of AMPK enhanced and gemcitabine-inhibited S6K expression. Conclusion: SLC39A1 contributed to gemcitabine resistance of PDAC by activating AMPK signaling.

scholarly journals High Expression of Cancer-Derived Glycosylated Immunoglobulin G Predicts Poor Prognosis in Pancreatic Ductal Adenocarcinoma

2020 ◽  
Vol 11 (8) ◽  
pp. 2213-2221
Author(s):  
Ming Cui ◽  
Lei You ◽  
Bang Zheng ◽  
Xinmei Huang ◽  
Qiaofei Liu ◽  
...  
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Immunoglobulin G ◽  
Poor Prognosis ◽  
High Expression ◽  
Ductal Adenocarcinoma

High expression of CDK1 and BUB1 predicts poor prognosis of pancreatic ductal adenocarcinoma

Gene ◽  
2019 ◽  
Vol 701 ◽  
pp. 15-22 ◽  
Author(s):  
Junjie Piao ◽  
Lianhua Zhu ◽  
Jie Sun ◽  
Nan Li ◽  
Bing Dong ◽  
...  
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Poor Prognosis ◽  
High Expression ◽  
Ductal Adenocarcinoma

scholarly journals Contribution of nuclear BCL10 expression to tumor progression and poor prognosis of advanced and/or metastatic pancreatic ductal adenocarcinoma by activating NF-κB-related signaling

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Sung-Hsin Kuo ◽  
Shih-Hung Yang ◽  
Ming-Feng Wei ◽  
Hsiao-Wei Lee ◽  
Yu-Wen Tien ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Progression ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cell Lines ◽  
Poor Prognosis ◽  
Cyclin B1 ◽  
Ductal Adenocarcinoma ◽  
Clinical Samples ◽  
Wild Type ◽  
Pdac Cell

Abstract Background We previously demonstrated that nuclear BCL10 translocation participates in the instigation of NF-κB in breast cancer and lymphoma cell lines. In this study, we assessed whether nuclear BCL10 translocation is clinically significant in advanced and metastatic pancreatic ductal adenocarcinoma (PDAC). Method and materials We analyzed the expression of BCL10-, cell cycle-, and NF-κB- related signaling molecules, and the DNA-binding activity of NF-κB in three PDAC cell lines (mutant KRAS lines: PANC-1 and AsPC-1; wild-type KRAS line: BxPC-3) using BCL10 short hairpin RNA (shBCL10). To assess the anti-tumor effect of BCL10 knockdown in PDAC xenograft model, PANC-1 cells treated with or without shBCL10 transfection were inoculated into the flanks of mice. We assessed the expression patterns of BCL10 and NF-κB in tumor cells in 136 patients with recurrent, advanced, and metastatic PDAC using immunohistochemical staining. Results We revealed that shBCL10 transfection caused cytoplasmic translocation of BCL10 from the nuclei, inhibited cell viability, and enhanced the cytotoxicities of gemcitabine and oxaliplatin in three PDAC cell lines. Inhibition of BCL10 differentially blocked cell cycle progression in PDAC cell lines. Arrest at G1 phase was noted in wild-type KRAS cell lines; and arrest at G2/M phase was noted in mutant KRAS cell lines. Furthermore, shBCL10 transfection downregulated the expression of phospho-CDC2, phospho-CDC25C, Cyclin B1 (PANC-1), Cyclins A, D1, and E, CDK2, and CDK4 (BxPC-3), p-IκBα, nuclear expression of BCL10, BCL3, and NF-κB (p65), and attenuated the NF-κB pathway activation and its downstream molecule, c-Myc, while inhibition of BCL10 upregulated expression of p21, and p27 in both PANC-1 and BxPC-3 cells. In a PANC-1-xenograft mouse model, inhibition of BCL10 expression also attenuated the tumor growth of PDAC. In clinical samples, nuclear BCL10 expression was closely associated with nuclear NF-κB expression (p < 0.001), and patients with nuclear BCL10 expression had the worse median overall survival than those without nuclear BCL10 expression (6.90 months versus 9.53 months, p = 0.019). Conclusion Nuclear BCL10 translocation activates NF-κB signaling and contributes to tumor progression and poor prognosis of advanced/metastatic PDAC.

High Expression of Interleukin-22 and Its Receptor Predicts Poor Prognosis in Pancreatic Ductal Adenocarcinoma

2013 ◽  
Vol 21 (1) ◽  
pp. 125-132 ◽  
Author(s):  
Zhang Wen ◽  
Quan Liao ◽  
Jianguo Zhao ◽  
Ya Hu ◽  
Lei You ◽  
...  
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Poor Prognosis ◽  
High Expression ◽  
Ductal Adenocarcinoma ◽  
Interleukin 22

scholarly journals High Expression of Cancer-Derived Glycosylated Immunoglobulin G Predicts Poor Prognosis in Pancreatic Ductal Adenocarcinoma: Erratum

2021 ◽  
Vol 12 (21) ◽  
pp. 6497-6497
Author(s):  
Ming Cui ◽  
Lei You ◽  
Bang Zheng ◽  
Xinmei Huang ◽  
Qiaofei Liu ◽  
...  
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Immunoglobulin G ◽  
Poor Prognosis ◽  
High Expression ◽  
Ductal Adenocarcinoma
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